首页 > 最新文献

Molecular Biology Research Communications最新文献

英文 中文
Association study of the polymorphisms rs2228611 of the DNMT1 gene and rs1569686 of the DNMT3B gene with bladder cancer development in a sample of the Algerian population. 阿尔及利亚人口样本中 DNMT1 基因 rs2228611 和 DNMT3B 基因 rs1569686 多态性与膀胱癌发病的关联研究。
IF 1.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/MBRC.2023.48569.1881
Zohra Touala-Chaila, Rym-Khadidja Abderrahmane, Slimane Kerroumi, Mostefa-Jamel Yousfi, Djebaria-Naima Meroufel, Abdallah Boudjema

Bladder cancer (BC) is a multifactorial disease with a poorly understood main cause. In this study, we aimed to evaluate the effect of the polymorphisms rs2228611 of the DNMT1 gene and rs1569686 of the DNMT3B gene on the susceptibility to develop Bladder Cancer in the Algerian population. A case-control study design was adopted, with DNA samples of 114 BC patients and 123 healthy controls. We found that the rs2228611 of the DNMT1 gene was strongly associated with an increased risk of BC development under genetic models: Codominant AG vs. GG (OR=2.54, 95% CI=1.21-5.51, adj p=0.015) and dominant AA+AG vs. GG (OR=2.24, 95% CI=1.12-4.60, adj p=0.023). However, no statistically significant association was observed between the rs1569686 of the DNMT3B gene and the predisposition to BC. To the best of our knowledge, this is the first peer-reviewed study to evaluate the effect of the rs2228611 polymorphism on bladder cancer occurrence. Our results suggest that the rs2228611 might be a potential biomarker for BC development risk. Additional studies are needed to validate our findings.

膀胱癌(BC)是一种多因素疾病,其主要病因尚不清楚。本研究旨在评估 DNMT1 基因 rs2228611 和 DNMT3B 基因 rs1569686 多态性对阿尔及利亚人群膀胱癌易感性的影响。研究采用病例对照设计,采集了 114 名膀胱癌患者和 123 名健康对照者的 DNA 样本。我们发现,在遗传模式下,DNMT1 基因的 rs2228611 与膀胱癌发病风险的增加密切相关:共显性 AG vs. GG(OR=2.54,95% CI=1.21-5.51,adj p=0.015)和显性 AA+AG vs. GG(OR=2.24,95% CI=1.12-4.60,adj p=0.023)。然而,在 DNMT3B 基因 rs1569686 与 BC 易感性之间未观察到有统计学意义的关联。据我们所知,这是第一项评估 rs2228611 多态性对膀胱癌发生影响的同行评审研究。我们的研究结果表明,rs2228611 可能是膀胱癌发病风险的潜在生物标志物。我们还需要更多的研究来验证我们的发现。
{"title":"Association study of the polymorphisms rs2228611 of the <i>DNMT1</i> gene and rs1569686 of the <i>DNMT3B</i> gene with bladder cancer development in a sample of the Algerian population.","authors":"Zohra Touala-Chaila, Rym-Khadidja Abderrahmane, Slimane Kerroumi, Mostefa-Jamel Yousfi, Djebaria-Naima Meroufel, Abdallah Boudjema","doi":"10.22099/MBRC.2023.48569.1881","DOIUrl":"https://doi.org/10.22099/MBRC.2023.48569.1881","url":null,"abstract":"<p><p>Bladder cancer (BC) is a multifactorial disease with a poorly understood main cause. In this study, we aimed to evaluate the effect of the polymorphisms rs2228611 of the DNMT1 gene and rs1569686 of the DNMT3B gene on the susceptibility to develop Bladder Cancer in the Algerian population. A case-control study design was adopted, with DNA samples of 114 BC patients and 123 healthy controls. We found that the rs2228611 of the DNMT1 gene was strongly associated with an increased risk of BC development under genetic models: Codominant AG <i>vs</i>. GG (OR=2.54, 95% CI=1.21-5.51, adj p=0.015) and dominant AA+AG <i>vs</i>. GG (OR=2.24, 95% CI=1.12-4.60, adj p=0.023). However, no statistically significant association was observed between the rs1569686 of the DNMT3B gene and the predisposition to BC. To the best of our knowledge, this is the first peer-reviewed study to evaluate the effect of the rs2228611 polymorphism on bladder cancer occurrence. Our results suggest that the rs2228611 might be a potential biomarker for BC development risk. Additional studies are needed to validate our findings.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 2","pages":"65-72"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10946547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140175673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells. miR-133a 在 Silibinin 介导的 MCF-7 乳腺癌细胞 PI3K/AKT/mTOR 通路抑制中的作用。
IF 1.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/MBRC.2024.48818.1903
Mohammadjavad Hossein-Tehrani, Roghayeh Abbasalipourkabir, Nasrin Ziamajidi

Breast cancer is particularly severe in women. Research highlights the crucial role of miRNAs in key cellular processes, showcasing their intricate interactions with the oncogenic PI3K/AKT/mTOR (PAM) signaling pathway and underscoring their significant role as tumor suppressors. The effect of silibinin on cell growth and survival was evaluated using an MTT assay. Bioinformatics analysis identified putative miR-133a targets inside the PAM pathway. After incubating MCF-7 cells with silibinin, we measured miR-133a, EGFR, PI3K, AKT, PTEN, and mTOR expression levels using qRT-PCR. Furthermore, protein expression levels of mTOR were assessed using Western blotting. The MTT experiment displayed that silibinin effectively inhibits MCF-7 cell proliferation in a time- and dose-dependent manner. Silibinin's IC50 value, determined at 370 μM after 48 hours, was established. qRT-PCR analysis at this IC50 concentration highlighted reduced expression of EGFR, PI3K, AKT, PTEN, and mTOR mRNAs, alongside increased miR-133a expression. Notably, miR-133a exhibited a negative correlation with both EGFR and PIK3C2A expression. Furthermore, western blotting confirmed silibinin's capacity to diminish p-mTOR protein levels, the ultimate element of the PAM signaling pathway. The findings enhance comprehension of silibinin's impact on PAM signaling and miR-133a expression, offering promise for targeted therapies in disrupting oncogenic pathways in MCF-7 breast cancer cells. This insight could advance breast cancer treatment strategies.

乳腺癌对女性的影响尤为严重。研究强调了 miRNA 在关键细胞过程中的重要作用,展示了它们与致癌的 PI3K/AKT/mTOR (PAM) 信号通路之间错综复杂的相互作用,并强调了它们作为肿瘤抑制因子的重要作用。使用 MTT 试验评估了西利宾对细胞生长和存活的影响。生物信息学分析确定了 PAM 通路中的推定 miR-133a 靶点。用 Silibinin 培养 MCF-7 细胞后,我们用 qRT-PCR 法测量了 miR-133a、表皮生长因子受体、PI3K、AKT、PTEN 和 mTOR 的表达水平。此外,我们还利用 Western 印迹技术评估了 mTOR 的蛋白表达水平。MTT实验表明,丝利宾能有效抑制MCF-7细胞的增殖,且具有时间和剂量依赖性。在此 IC50 浓度下进行的 qRT-PCR 分析显示,表皮生长因子受体、PI3K、AKT、PTEN 和 mTOR mRNA 的表达减少,miR-133a 的表达增加。值得注意的是,miR-133a 与表皮生长因子受体和 PIK3C2A 的表达呈负相关。此外,Western 印迹证实西利宾能够降低 p-mTOR 蛋白水平,而 p-mTOR 蛋白是 PAM 信号通路的最终元素。这些发现加深了人们对西利宾对PAM信号转导和miR-133a表达的影响的理解,为破坏MCF-7乳腺癌细胞致癌途径的靶向疗法提供了希望。这一发现将推动乳腺癌治疗策略的发展。
{"title":"The role of miR-133a in silibinin-mediated inhibition of the PI3K/AKT/mTOR pathway in MCF-7 breast carcinoma cells.","authors":"Mohammadjavad Hossein-Tehrani, Roghayeh Abbasalipourkabir, Nasrin Ziamajidi","doi":"10.22099/MBRC.2024.48818.1903","DOIUrl":"https://doi.org/10.22099/MBRC.2024.48818.1903","url":null,"abstract":"<p><p>Breast cancer is particularly severe in women. Research highlights the crucial role of miRNAs in key cellular processes, showcasing their intricate interactions with the oncogenic PI3K/AKT/mTOR (PAM) signaling pathway and underscoring their significant role as tumor suppressors. The effect of silibinin on cell growth and survival was evaluated using an MTT assay. Bioinformatics analysis identified putative miR-133a targets inside the PAM pathway. After incubating MCF-7 cells with silibinin, we measured miR-133a, <i>EGFR</i>, <i>PI3K</i>, <i>AKT</i>, <i>PTEN</i>, and <i>mTOR</i> expression levels using qRT-PCR. Furthermore, protein expression levels of mTOR were assessed using Western blotting. The MTT experiment displayed that silibinin effectively inhibits MCF-7 cell proliferation in a time- and dose-dependent manner. Silibinin's IC<sub>50</sub> value, determined at 370 μM after 48 hours, was established. qRT-PCR analysis at this IC<sub>50</sub> concentration highlighted reduced expression of <i>EGFR</i>, <i>PI3K</i>, <i>AKT</i>, <i>PTEN</i>, and <i>mTOR</i> mRNAs, alongside increased miR-133a expression. Notably, miR-133a exhibited a negative correlation with both <i>EGFR</i> and <i>PIK3C2A</i> expression. Furthermore, western blotting confirmed silibinin's capacity to diminish p-mTOR protein levels, the ultimate element of the PAM signaling pathway. The findings enhance comprehension of silibinin's impact on PAM signaling and miR-133a expression, offering promise for targeted therapies in disrupting oncogenic pathways in MCF-7 breast cancer cells. This insight could advance breast cancer treatment strategies.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 2","pages":"79-83"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10946549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140175678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Comparison of inflammatory molecular mechanisms between osteoarthritis and rheumatoid arthritis via gene microarrays. 通过基因芯片比较骨关节炎和类风湿关节炎的炎症分子机制。
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.49924.1963
Maziar Oveisee, Akram Gholipour, Mahshid Malakootian

Osteoarthritis (OA) and rheumatoid arthritis (RA) treatment requires exact arthritis type diagnosis. We compared inflammatory molecular mechanisms between OA and RA to introduce reliable molecular biomarkers. The GSE55235 and GSE100786 microarray datasets were acquired from the GEO. Data preprocessing and differential expression analysis were conducted in OA and RA groups and their control groups applying GEO2R. Differentially expressed genes (DEGs) with a |LogFC|>1 and adj. p<0.05 were determined. Gene ontology (GO) and signaling pathway analysis were done utilizing PANTHER and Enrichr. The suitability of gene expression alterations as biomarkers was tested using the receiver operating characteristic (ROC) curve analysis. We found 2129 DEGs between the OA and control groups and 2494 DEGs between the RA and control groups. GO on the DEGs showed enrichment in binding, cellular processes, and cellular anatomical entities in molecular functions, biological processes, and cellular components, respectively. Enrichr found the cell differentiation pathways of Th1 and Th2 only in RA. The ROC curve analysis indicated HLA-DQA1 downregulation and MAPK8IP3 upregulation as reliable biomarkers to discriminate RA from OA in peripheral blood and bone marrow samples, respectively. We found more DEGs in patients with OA than those with RA and determined inflammatory pathways and genes unique to RA as reliable biomarkers to discriminate RA from OA. Gene expression alterations associated with Th1 and Th2 cell differentiation pathways, including HLA-DQA1 downregulation and MAPK8IP3 upregulation, could be novel molecular biomarkers to diagnose RA.

骨关节炎(OA)和类风湿性关节炎(RA)的治疗需要准确的关节炎类型诊断。我们比较了 OA 和 RA 的炎症分子机制,以引入可靠的分子生物标记物。我们从 GEO 获取了 GSE55235 和 GSE100786 微阵列数据集。应用 GEO2R 对 OA 组和 RA 组及其对照组进行数据预处理和差异表达分析。在外周血和骨髓样本中,差异表达基因(DEGs)的|LogFC|>1和adj.pHLA-DQA1下调和MAPK8IP3上调分别是区分RA和OA的可靠生物标志物。我们在OA患者中发现了比RA患者更多的DEGs,并确定了RA特有的炎症通路和基因作为鉴别RA和OA的可靠生物标志物。与Th1和Th2细胞分化途径相关的基因表达改变,包括HLA-DQA1下调和MAPK8IP3上调,可能成为诊断RA的新型分子生物标记物。
{"title":"Comparison of inflammatory molecular mechanisms between osteoarthritis and rheumatoid arthritis via gene microarrays.","authors":"Maziar Oveisee, Akram Gholipour, Mahshid Malakootian","doi":"10.22099/mbrc.2024.49924.1963","DOIUrl":"10.22099/mbrc.2024.49924.1963","url":null,"abstract":"<p><p>Osteoarthritis (OA) and rheumatoid arthritis (RA) treatment requires exact arthritis type diagnosis. We compared inflammatory molecular mechanisms between OA and RA to introduce reliable molecular biomarkers. The GSE55235 and GSE100786 microarray datasets were acquired from the GEO. Data preprocessing and differential expression analysis were conducted in OA and RA groups and their control groups applying GEO2R. Differentially expressed genes (DEGs) with a |LogFC|>1 and adj. <i>p</i><0.05 were determined. Gene ontology (GO) and signaling pathway analysis were done utilizing PANTHER and Enrichr. The suitability of gene expression alterations as biomarkers was tested using the receiver operating characteristic (ROC) curve analysis. We found 2129 DEGs between the OA and control groups and 2494 DEGs between the RA and control groups. GO on the DEGs showed enrichment in binding, cellular processes, and cellular anatomical entities in molecular functions, biological processes, and cellular components, respectively. Enrichr found the cell differentiation pathways of Th1 and Th2 only in RA. The ROC curve analysis indicated <i>HLA-DQA1</i> downregulation and <i>MAPK8IP3</i> upregulation as reliable biomarkers to discriminate RA from OA in peripheral blood and bone marrow samples, respectively. We found more DEGs in patients with OA than those with RA and determined inflammatory pathways and genes unique to RA as reliable biomarkers to discriminate RA from OA. Gene expression alterations associated with Th1 and Th2 cell differentiation pathways, including <i>HLA-DQA1</i> downregulation and <i>MAPK8IP3</i> upregulation, could be novel molecular biomarkers to diagnose RA.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 4","pages":"211-222"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clinical profile of FTL3-ITD mutation in West Algerian population with acute myeloid leukemia. 西阿尔及利亚急性髓性白血病患者FTL3-ITD突变的临床概况。
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.49437.1955
Fatima Zohra Moghtit, Wefa Boughrara, Samia Dorgham, Ilies Koriche, Imene Ouahba, Amina Ammour, Amine Bekadja, Meriem Samia Aberkane

Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the abnormal and rapid growth of cells. The mutation of the Fms-like tyrosine kinase 3 ligand gene (FLT3-ITD) represents an important factor in the prognosis of AML. The objective of this study was to determine for the first time the prevalence of FLT3-ITD mutation in west Algerian AML patients. A total of 160 AML patients were genotyped for FLT3-ITD mutation by using polymerase chain reaction. FLT3-ITD mutation was detected in 13% of patients. Mutation rates show no significant difference in the distribution of sex and age. A positive association was found between this mutation and a higher leukocyte and blast cells counts. We also found that the M3 and M5 subtype were the commonest in the FLT3 mutated group. This preliminary study provides first-time prevalence estimates for FLT3-ITD mutation in acute myeloid leukemia patients from the West region of Algeria.

急性髓性白血病(AML)是一种髓系血细胞癌症,其特点是细胞异常快速生长。Fms 样酪氨酸激酶 3 配体基因(FLT3-ITD)的突变是影响急性髓性白血病预后的一个重要因素。本研究旨在首次确定FLT3-ITD基因突变在阿尔及利亚西部急性髓细胞性白血病患者中的流行率。研究人员利用聚合酶链反应对 160 名急性髓细胞性白血病患者进行了 FLT3-ITD 基因突变的基因分型。13%的患者检测到FLT3-ITD突变。突变率在性别和年龄分布上无明显差异。这种突变与较高的白细胞和囊细胞计数之间存在正相关。我们还发现,M3 和 M5 亚型在 FLT3 突变组中最为常见。这项初步研究首次估计了阿尔及利亚西部地区急性髓性白血病患者中FLT3-ITD突变的流行率。
{"title":"Clinical profile of <i>FTL3</i>-ITD mutation in West Algerian population with acute myeloid leukemia.","authors":"Fatima Zohra Moghtit, Wefa Boughrara, Samia Dorgham, Ilies Koriche, Imene Ouahba, Amina Ammour, Amine Bekadja, Meriem Samia Aberkane","doi":"10.22099/mbrc.2024.49437.1955","DOIUrl":"10.22099/mbrc.2024.49437.1955","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the abnormal and rapid growth of cells. The mutation of the Fms-like tyrosine kinase 3 ligand gene (<i>FLT3</i>-ITD) represents an important factor in the prognosis of AML. The objective of this study was to determine for the first time the prevalence of <i>FLT3</i>-ITD mutation in west Algerian AML patients. A total of 160 AML patients were genotyped for <i>FLT3</i>-ITD mutation by using polymerase chain reaction. <i>FLT3</i>-ITD mutation was detected in 13% of patients. Mutation rates show no significant difference in the distribution of sex and age. A positive association was found between this mutation and a higher leukocyte and blast cells counts. We also found that the M3 and M5 subtype were the commonest in the <i>FLT3</i> mutated group. This preliminary study provides first-time prevalence estimates for <i>FLT3</i>-ITD mutation in acute myeloid leukemia patients from the West region of Algeria.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"175-182"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Natural compounds solasonine and alisol B23-acetate target GLI3 signaling to block oncogenesis in MED12-altered breast cancer. 天然化合物 Solasonine 和 alisol B23-acetate 以 GLI3 信号为靶点,阻断 MED12 改变的乳腺癌的致癌过程。
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.49044.1915
Shivani Akula, Cristian G Gonzalez, Sophia Kermet, Marieke Burleson

Breast cancer remains to be the second leading cause of cancer deaths worldwide thereby highlighting the critical need to find superior treatment strategies for this disease. In the current era of cancer treatment, personalized medicine is garnering much attention as this type of treatment is more selective thereby minimizing harmful side effects. Personalized medicine is dependent upon knowing the underlying genetic landscape of the initial tumor. In our study, we focused our efforts on a specific subset of breast cancer that harbors genetic alterations in the Mediator subunit 12 (MED12). Our results show that loss of MED12 leads to enhanced cellular proliferation and colony formation of breast cancer cells through a mechanism that involves activation of GLI3-dependent SHH signaling, a pathway that is central to breast development and homeostasis. To find a personalized treatment option for this subset of breast cancer, we employed a natural compound screening strategy which uncovered a total of ten compounds that selectively target MED12 knockdown breast cancer cells. Our results show that two of these ten compounds, solasonine and alisol B23-acetate, block GLI3-dependent SHH signaling which leads to a reversal of enhanced cellular proliferation and colony formation ability. Thus, our findings provide promising insight into a novel personalized treatment strategy for patients suffering from MED12-altered breast cancer.

乳腺癌仍然是全球癌症死亡的第二大原因,因此迫切需要找到治疗这种疾病的最佳策略。在当前的癌症治疗时代,个性化医疗备受关注,因为这种治疗方法更具选择性,从而最大限度地减少了有害的副作用。个性化医疗依赖于了解初始肿瘤的潜在基因状况。在我们的研究中,我们重点研究了乳腺癌的一个特定亚群,该亚群中的介导子亚基 12(MED12)存在基因改变。我们的研究结果表明,MED12 的缺失会导致乳腺癌细胞的细胞增殖和集落形成增强,其机制涉及到 GLI3 依赖性 SHH 信号的激活,而 SHH 信号是乳腺发育和平衡的核心通路。为了找到针对这一乳腺癌亚群的个性化治疗方案,我们采用了一种天然化合物筛选策略,共发现了十种可选择性靶向 MED12 基因敲除乳腺癌细胞的化合物。我们的研究结果表明,这十种化合物中的两种--索拉宁(solasonine)和阿利索 B23-乙酸酯(alisol B23-acetate)--能阻断依赖于 GLI3 的 SHH 信号转导,从而逆转增强的细胞增殖和集落形成能力。因此,我们的研究结果有望为MED12改变的乳腺癌患者提供一种新型的个性化治疗策略。
{"title":"Natural compounds solasonine and alisol B23-acetate target GLI3 signaling to block oncogenesis in MED12-altered breast cancer.","authors":"Shivani Akula, Cristian G Gonzalez, Sophia Kermet, Marieke Burleson","doi":"10.22099/mbrc.2024.49044.1915","DOIUrl":"10.22099/mbrc.2024.49044.1915","url":null,"abstract":"<p><p>Breast cancer remains to be the second leading cause of cancer deaths worldwide thereby highlighting the critical need to find superior treatment strategies for this disease. In the current era of cancer treatment, personalized medicine is garnering much attention as this type of treatment is more selective thereby minimizing harmful side effects. Personalized medicine is dependent upon knowing the underlying genetic landscape of the initial tumor. In our study, we focused our efforts on a specific subset of breast cancer that harbors genetic alterations in the Mediator subunit 12 (MED12). Our results show that loss of MED12 leads to enhanced cellular proliferation and colony formation of breast cancer cells through a mechanism that involves activation of GLI3-dependent SHH signaling, a pathway that is central to breast development and homeostasis. To find a personalized treatment option for this subset of breast cancer, we employed a natural compound screening strategy which uncovered a total of ten compounds that selectively target MED12 knockdown breast cancer cells. Our results show that two of these ten compounds, solasonine and alisol B23-acetate, block GLI3-dependent SHH signaling which leads to a reversal of enhanced cellular proliferation and colony formation ability. Thus, our findings provide promising insight into a novel personalized treatment strategy for patients suffering from MED12-altered breast cancer.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"127-135"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MicroRNAs targeting CDKN2A gene as a potential prognostic marker in head and neck squamous cell carcinoma. 靶向 CDKN2A 基因的微小 RNA 是头颈部鳞状细胞癌的潜在预后标志物。
IF 1.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2023.48081.1853
Sivakumar Gopalakrishnan, Anitha Pandi, Paramasivam Arumugam, Vijayashree Priyadharsini Jayaseelan

Epigenetic factors are known to markedly influence the functions of a gene by modification of transcripts, via methylation or acetylation and degradation of mRNA transcripts. The CDKN2A encodes cyclin-dependent kinase inhibitor 2A, a tumour suppressor protein. Genetic and epigenetic alterations in this gene have been demonstrated in several cancer types. The non-coding RNAs with a special emphasis on microRNAs have long been explored for their potential role in the epigenetic modification of gene expression. The present study aims to identify the microRNAs targeting CDKN2A gene transcripts and demonstrate their prognostic significance in head and neck squamous cell carcinoma (HNSCC). Computational approaches were employed to identify the microRNAs targeting CDKN2A. The gene and protein expression profile of CDKN2A was analyzed using UALCAN. A significant upregulation of CDKN2A was observed in the primary tumour tissues (p=<10-12). Interestingly, the protein expression, although found to be statistically significant (p=0.0129) did not correlate well with the gene expression profile. The microRNAs targeting CDKN2A were further analyzed to identify the possible reason for the decrease in protein expression. Among the 44 microRNAs targeting CDKN2A gene transcripts, hsa-miR-3681-3p, hsa-miR-542-5p, hsa-miR-4519 were found to be upregulated and hsa-miR-134-5p was found to be downregulated with a significant association with survival status of HNSCC patients. The hsa-miR-542-5p was found to correlate well with the survival and hence can be considered as the key microRNA associated with HNSCC. However, further validation of this microRNA is warranted to confirm its role in the process of carcinogenesis.

众所周知,表观遗传因子通过甲基化或乙酰化以及 mRNA 转录本的降解来修饰转录本,从而显著影响基因的功能。CDKN2A 编码细胞周期蛋白依赖性激酶抑制剂 2A,是一种肿瘤抑制蛋白。该基因的遗传和表观遗传学改变已在几种癌症类型中得到证实。长期以来,人们一直在探索非编码 RNA,特别是 microRNA 在基因表达的表观遗传学改变中的潜在作用。本研究旨在鉴定靶向 CDKN2A 基因转录本的 microRNAs,并证明它们在头颈部鳞状细胞癌(HNSCC)中的预后意义。研究人员采用计算方法鉴定了靶向 CDKN2A 的 microRNA。利用 UALCAN 分析了 CDKN2A 的基因和蛋白表达谱。在原发性肿瘤组织中观察到 CDKN2A 明显上调(p=-12)。有趣的是,蛋白质表达虽然具有统计学意义(p=0.0129),但与基因表达谱并不十分相关。我们进一步分析了靶向 CDKN2A 的 microRNA,以确定蛋白表达下降的可能原因。在44个靶向CDKN2A基因转录物的microRNA中,发现hsa-miR-3681-3p、hsa-miR-542-5p和hsa-miR-4519被上调,而hsa-miR-134-5p被下调,且与HNSCC患者的生存状况有显著关联。研究发现,hsa-miR-542-5p 与存活率密切相关,因此可被视为与 HNSCC 相关的关键微RNA。不过,还需要对该微RNA进行进一步验证,以确认其在癌变过程中的作用。
{"title":"MicroRNAs targeting <i>CDKN2A</i> gene as a potential prognostic marker in head and neck squamous cell carcinoma.","authors":"Sivakumar Gopalakrishnan, Anitha Pandi, Paramasivam Arumugam, Vijayashree Priyadharsini Jayaseelan","doi":"10.22099/mbrc.2023.48081.1853","DOIUrl":"10.22099/mbrc.2023.48081.1853","url":null,"abstract":"<p><p>Epigenetic factors are known to markedly influence the functions of a gene by modification of transcripts, <i>via</i> methylation or acetylation and degradation of mRNA transcripts. The <i>CDKN2A</i> encodes cyclin-dependent kinase inhibitor 2A, a tumour suppressor protein. Genetic and epigenetic alterations in this gene have been demonstrated in several cancer types. The non-coding RNAs with a special emphasis on microRNAs have long been explored for their potential role in the epigenetic modification of gene expression. The present study aims to identify the microRNAs targeting <i>CDKN2A</i> gene transcripts and demonstrate their prognostic significance in head and neck squamous cell carcinoma (HNSCC). Computational approaches were employed to identify the microRNAs targeting <i>CDKN2A.</i> The gene and protein expression profile of <i>CDKN2A</i> was analyzed using UALCAN. A significant upregulation of <i>CDKN2A</i> was observed in the primary tumour tissues (p=<10<sup>-12</sup>). Interestingly, the protein expression, although found to be statistically significant (p=0.0129) did not correlate well with the gene expression profile. The microRNAs targeting <i>CDKN2A</i> were further analyzed to identify the possible reason for the decrease in protein expression. Among the 44 microRNAs targeting <i>CDKN2A</i> gene transcripts, hsa-miR-3681-3p, hsa-miR-542-5p, hsa-miR-4519 were found to be upregulated and hsa-miR-134-5p was found to be downregulated with a significant association with survival status of HNSCC patients. The hsa-miR-542-5p was found to correlate well with the survival and hence can be considered as the key microRNA associated with HNSCC. However, further validation of this microRNA is warranted to confirm its role in the process of carcinogenesis.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 1","pages":"21-27"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Valproic acid and/or rapamycin preconditioning protects hair follicle stem cells from oxygen glucose serum deprivation-induced oxidative injury via activating Nrf2 pathway. 丙戊酸和/或雷帕霉素预处理通过激活Nrf2通路保护毛囊干细胞免受氧葡萄糖血清剥夺诱导的氧化损伤。
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.49302.1922
Fatemeh Keshavarzi, Mohammad Saied Salehi, Sareh Pandamooz, Razieh Zare, Mozhdeh Zamani, Zohreh Mostafavi-Pour, Pooneh Pooneh Mokarram

Among leading causes of the ischemic stroke pathogenesis, oxidative stress strongly declines rate of stem cell engraftment at the injury site, and disables stem cell-based therapy as a key treatment for ischemia stroke. To overcome this therapeutic limitation, preconditioning has been represented a possible approach to augment the adaptation and viability of stem cells to oxidative stress. Here, we illustrated protective impacts of valproic acid (VPA) and/or rapamycin (RAPA) preconditioning unto oxygen glucose and serum deprivation (OGSD)-stimulated cell damage in hair follicle-derived stem cells (HFSCs) and surveyed the plausible inducement mechanisms. OGSD, as an in vitro cell injury model, was established and HFSCs viability was observed using MTT assay after VPA, RAPA, and VPA-RAPA preconditioning under OGSD. ROS and MDA production was assessed to reflect oxidative stress. Real-time PCR and western blotting were employed to investigate Nrf2 expression. The activity of Nrf2-related antioxidant enzymes including NQO1, GPx and GSH level were examined. VEGF and BDNF mRNA expression levels were analyzed. Our results showed that VPA and/or RAPA preconditioning ameliorated OGSD-induced decline in HFSCs viability. In addition, they considerably prohibited ROS and MDA generation in the OGSD-treated HFSCs. Furthermore, VPA and/or RAPA preconditioning stimulated Nrf2 nuclear repositioning and NQO1 and GPx activity and GSH amount, as well as expression of paracrine factors VEGF and BDNF in OGSD-treated HFSCs. Thus, the protective effects afforded by VPA and/or RAPA preconditioning, which involved Nrf2-modulated oxidant stress and regulation of VEGF and BDNF expression, display a simple strategy to augment cell-transplantation efficiency for ischemic stroke.

在缺血性中风发病机制的主要原因中,氧化应激大大降低了干细胞在损伤部位的移植率,使干细胞疗法无法成为缺血性中风的主要治疗方法。为了克服这一治疗限制,预处理被认为是增强干细胞对氧化应激的适应性和活力的一种可能方法。在这里,我们说明了丙戊酸(VPA)和/或雷帕霉素(RAPA)预处理对氧葡萄糖和血清剥夺(OGSD)刺激的毛囊干细胞(HFSCs)细胞损伤的保护性影响,并研究了合理的诱导机制。建立了体外细胞损伤模型 OGSD,并在 OGSD 条件下使用 MTT 法观察 VPA、RAPA 和 VPA-RAPA 预处理后毛囊干细胞的存活率。评估 ROS 和 MDA 的产生以反映氧化应激。实时 PCR 和 Western 印迹技术用于研究 Nrf2 的表达。检测了 Nrf2 相关抗氧化酶的活性,包括 NQO1、GPx 和 GSH 水平。分析了血管内皮生长因子和 BDNF mRNA 的表达水平。结果表明,VPA和/或RAPA预处理可改善OGSD诱导的高频间充质干细胞活力下降。此外,它们还大大抑制了 ROS 和 MDA 在 OGSD 处理的高频间充质干细胞中的生成。此外,VPA 和/或 RAPA 预处理刺激了 Nrf2 核重新定位、NQO1 和 GPx 活性、GSH 含量,以及辅助因子 VEGF 和 BDNF 在 OGSD 处理的高频间充质干细胞中的表达。因此,VPA和/或RAPA预处理提供的保护作用涉及Nrf2调节的氧化应激以及VEGF和BDNF表达的调节,是提高缺血性脑卒中细胞移植效率的一种简单策略。
{"title":"Valproic acid and/or rapamycin preconditioning protects hair follicle stem cells from oxygen glucose serum deprivation-induced oxidative injury via activating Nrf2 pathway.","authors":"Fatemeh Keshavarzi, Mohammad Saied Salehi, Sareh Pandamooz, Razieh Zare, Mozhdeh Zamani, Zohreh Mostafavi-Pour, Pooneh Pooneh Mokarram","doi":"10.22099/mbrc.2024.49302.1922","DOIUrl":"10.22099/mbrc.2024.49302.1922","url":null,"abstract":"<p><p>Among leading causes of the ischemic stroke pathogenesis, oxidative stress strongly declines rate of stem cell engraftment at the injury site, and disables stem cell-based therapy as a key treatment for ischemia stroke. To overcome this therapeutic limitation, preconditioning has been represented a possible approach to augment the adaptation and viability of stem cells to oxidative stress. Here, we illustrated protective impacts of valproic acid (VPA) and/or rapamycin (RAPA) preconditioning unto oxygen glucose and serum deprivation (OGSD)-stimulated cell damage in hair follicle-derived stem cells (HFSCs) and surveyed the plausible inducement mechanisms. OGSD, as an <i>in vitro</i> cell injury model, was established and HFSCs viability was observed using MTT assay after VPA, RAPA, and VPA-RAPA preconditioning under OGSD. ROS and MDA production was assessed to reflect oxidative stress. Real-time PCR and western blotting were employed to investigate Nrf2 expression. The activity of Nrf2-related antioxidant enzymes including NQO1, GPx and GSH level were examined. <i>VEGF</i> and <i>BDNF</i> mRNA expression levels were analyzed. Our results showed that VPA and/or RAPA preconditioning ameliorated OGSD-induced decline in HFSCs viability. In addition, they considerably prohibited ROS and MDA generation in the OGSD-treated HFSCs. Furthermore, VPA and/or RAPA preconditioning stimulated Nrf2 nuclear repositioning and NQO1 and GPx activity and GSH amount, as well as expression of paracrine factors <i>VEGF</i> and <i>BDNF</i> in OGSD-treated HFSCs. Thus, the protective effects afforded by VPA and/or RAPA preconditioning, which involved Nrf2-modulated oxidant stress and regulation of <i>VEGF</i> and <i>BDNF</i> expression, display a simple strategy to augment cell-transplantation efficiency for ischemic stroke.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"103-116"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Allele and genotype frequencies of β-lactoglobulin gene using PCR-RFLP in Algerian local cattle populations. 利用 PCR-RFLP 技术测定阿尔及利亚当地牛群中 β 乳球蛋白基因的等位基因和基因型频率。
IF 1.6 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2023.47661.1841
Nadjet Boushaba, Nacera Tabet-Aoul

Milk protein genetic polymorphisms are associated with economically important traits in dairy cattle. The objective of this study is to genotype a single nucleotide polymorphism (SNP) responsible for the amino acid changes in the beta-lactoglobulin (β-Lg) variants A and B on 85 unrelated DNA representing Algerian cattle populations: Chelifienne (28), Cheurfa (31) and Guelmoise (26). The method used is the PCR-RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism). Genetic polymorphism was detected by digestion of PCR products amplified of exon II of β-Lg gene by with the endonuclease HaeIII enzyme. The results revealed that the amplified product was observed as 247 bp. Restriction digestion with HaeIII revealed three genotypes: AA, AB and BB. The genotypic frequencies of AA, AB and BB genotypes were 0.08, 0.41, 0.50; 0.08, 0.41, 0.50 and 0.01, 0.19, 0.56 in Chelifienne, Cheurfa and Guelmoise and respectively. Frequency of AA genotype was absent in Guelmoise population. Frequencies of A and B alleles were 0.29 and 0.71 in both Chelifienne and Cheurfa and 0.25 and 0.75 Guelmoise population. These results further confirm that Bos torus cattle are predominantly of β-Lactoglobulin B type. The Chi-square test at p-value < 0.05 results revealed that the Chelifienne and Cheurfa populations were in Hardy-Weinberg equilibrium and the results are not significant for the Guelmoise. This genetic information could be useful to estimate the effect of polymorphism on different milk production of Algerian bovine populations.

乳蛋白基因多态性与奶牛的重要经济性状有关。本研究的目的是对代表阿尔及利亚牛种群的 85 个无关联 DNA 上的β-乳球蛋白(β-Lg)变体 A 和 B 的氨基酸变化负责的单核苷酸多态性(SNP)进行基因分型:Chelifienne(28)、Cheurfa(31)和 Guelmoise(26)。使用的方法是 PCR-RFLP(聚合酶链式反应-限制性片段长度多态性)。用内切酶 HaeIII 消化β-Lg 基因外显子 II 的 PCR 扩增产物,检测基因多态性。结果显示,扩增产物为 247 bp。用 HaeIII 进行限制性消化发现了三种基因型:AA、AB 和 BB:AA、AB 和 BB。在 Chelifienne、Cheurfa 和 Guelmoise,AA、AB 和 BB 基因型的频率分别为 0.08、0.41、0.50;0.08、0.41、0.50 和 0.01、0.19、0.56。Guelmoise人群中没有AA基因型。A和B等位基因在Chelifienne和Cheurfa种群中的频率分别为0.29和0.71,在Guelmoise种群中的频率分别为0.25和0.75。这些结果进一步证实,Bos torus 牛主要属于 β-乳球蛋白 B 型。P值<0.05的Chi-square检验结果显示,Chelifienne种群和Cheurfa种群处于Hardy-Weinberg平衡状态,而Guelmoise种群的结果并不显著。这些遗传信息有助于估计多态性对阿尔及利亚牛群不同产奶量的影响。
{"title":"Allele and genotype frequencies of β-lactoglobulin gene using PCR-RFLP in Algerian local cattle populations.","authors":"Nadjet Boushaba, Nacera Tabet-Aoul","doi":"10.22099/mbrc.2023.47661.1841","DOIUrl":"10.22099/mbrc.2023.47661.1841","url":null,"abstract":"<p><p>Milk protein genetic polymorphisms are associated with economically important traits in dairy cattle. The objective of this study is to genotype a single nucleotide polymorphism (SNP) responsible for the amino acid changes in the beta-lactoglobulin (β-Lg) variants A and B on 85 unrelated DNA representing Algerian cattle populations: Chelifienne (28), Cheurfa (31) and Guelmoise (26). The method used is the PCR-RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism). Genetic polymorphism was detected by digestion of PCR products amplified of exon II of β-Lg gene by with the endonuclease <i>Hae</i>III enzyme. The results revealed that the amplified product was observed as 247 bp. Restriction digestion with <i>Hae</i>III revealed three genotypes: AA, AB and BB. The genotypic frequencies of AA, AB and BB genotypes were 0.08, 0.41, 0.50; 0.08, 0.41, 0.50 and 0.01, 0.19, 0.56 in Chelifienne, Cheurfa and Guelmoise and respectively. Frequency of AA genotype was absent in Guelmoise population. Frequencies of A and B alleles were 0.29 and 0.71 in both Chelifienne and Cheurfa and 0.25 and 0.75 Guelmoise population. These results further confirm that Bos torus cattle are predominantly of β-Lactoglobulin B type. The Chi-square test at <i>p</i>-value < 0.05 results revealed that the Chelifienne and Cheurfa populations were in Hardy-Weinberg equilibrium and the results are not significant for the Guelmoise. This genetic information could be useful to estimate the effect of polymorphism on different milk production of Algerian bovine populations.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 1","pages":"43-49"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of silymarin as adjuvant drug on serum levels of CTRP3, anti-cyclic citrullinated peptide (CCP), and high-sensitivity C-reactive protein (hs-CRP) in rheumatoid arthritis patients. 水飞蓟素作为辅助药物对类风湿性关节炎患者血清中 CTRP3、抗环瓜氨酸肽 (CCP) 和高敏 C 反应蛋白 (hs-CRP) 水平的影响。
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.48466.1876
Mohammad Ehsan Elahi, Daniel Elieh-Ali-Komi, Farjam Goudarzi, Ehsan Mohammadi Noori, Shirin Assar, Mehrdad Shavandi, Amir Kiani, Homayoin Elahi

Silymarin is known for its anti-inflammatory and antioxidant properties. We investigated these effects on serum levels of CTRP3, Anti-CCP, and hs-CRP in individuals with Rheumatoid arthritis (RA). In this study, 42 individuals with RA were recruited and their serum specimens were collected, serum levels of hs-CRP, AntiCCP antibodies, and CTRP3 were measured using ELISA. DNA was extracted and investigated for the existence of possible new mutations in the gene encoding CTRP3 using the PCR technique; the desired fragments were then amplified and sequenced. Another blood sample was collected from the case group after taking livergol for three months (3 doses of 140 mg/day) and the tests were repeated. Anti-CCP Abs levels in the postintervention responding group decreased compared to preintervention (p<0.001) while in the non-responding group, the levels increased after the intervention compared to the levels before the intervention (p=0.019). Additionally, CTRP3 levels in the responding group increased postintervention (p=0.003), however, in the non-responding group the levels decreased postintervention when compared to preintervention (p=0.02). The responding group had significantly lower levels of hs-CRP when compared to that of preintervention (p=0.005) whereas the non-responding group had significantly higher levels of postintervention (p<0.001). Moreover, the results of sequencings of exon 6 on CTRP3 gene showed the presence of mutations in exon 6 (position 215:C>T, 338:G>A, 359:A>C, and 153:T>C). Silymarin could be used as an adjuvant in the treatment of rheumatoid arthritis.

水飞蓟素以其抗炎和抗氧化特性而闻名。我们研究了水飞蓟素对类风湿关节炎(RA)患者血清中 CTRP3、Anti-CCP 和 hs-CRP 水平的影响。在这项研究中,我们招募了 42 名类风湿性关节炎患者,收集了他们的血清标本,并使用 ELISA 方法测量了血清中 hs-CRP、AntiCCP 抗体和 CTRP3 的水平。提取 DNA,利用 PCR 技术检测编码 CTRP3 的基因中是否存在可能的新突变;然后对所需片段进行扩增和测序。病例组在服用肝胆宁三个月(3 次,每次 140 毫克/天)后采集了另一份血液样本,并重复进行了检测。与干预前相比,干预后反应组的抗 CCP 抗原水平有所下降(pCTRP3 基因显示第 6 外显子存在突变(位置 215:C>T、338:G>A、359:A>C 和 153:T>C)。水飞蓟素可作为治疗类风湿性关节炎的辅助药物。
{"title":"Effects of silymarin as adjuvant drug on serum levels of CTRP3, anti-cyclic citrullinated peptide (CCP), and high-sensitivity C-reactive protein (hs-CRP) in rheumatoid arthritis patients.","authors":"Mohammad Ehsan Elahi, Daniel Elieh-Ali-Komi, Farjam Goudarzi, Ehsan Mohammadi Noori, Shirin Assar, Mehrdad Shavandi, Amir Kiani, Homayoin Elahi","doi":"10.22099/mbrc.2024.48466.1876","DOIUrl":"10.22099/mbrc.2024.48466.1876","url":null,"abstract":"<p><p>Silymarin is known for its anti-inflammatory and antioxidant properties. We investigated these effects on serum levels of CTRP3, Anti-CCP, and hs-CRP in individuals with Rheumatoid arthritis (RA). In this study, 42 individuals with RA were recruited and their serum specimens were collected, serum levels of hs-CRP, AntiCCP antibodies, and CTRP3 were measured using ELISA. DNA was extracted and investigated for the existence of possible new mutations in the gene encoding CTRP3 using the PCR technique; the desired fragments were then amplified and sequenced. Another blood sample was collected from the case group after taking <i>livergol</i> for three months (3 doses of 140 mg/day) and the tests were repeated. Anti-CCP Abs levels in the postintervention responding group decreased compared to preintervention (p<0.001) while in the non-responding group, the levels increased after the intervention compared to the levels before the intervention (p=0.019). Additionally, CTRP3 levels in the responding group increased postintervention (p=0.003), however, in the non-responding group the levels decreased postintervention when compared to preintervention (p=0.02). The responding group had significantly lower levels of hs-CRP when compared to that of preintervention (p=0.005) whereas the non-responding group had significantly higher levels of postintervention (p<0.001). Moreover, the results of sequencings of exon 6 on <i>CTRP3</i> gene showed the presence of mutations in exon 6 (position 215:C>T, 338:G>A, 359:A>C, and 153:T>C). Silymarin could be used as an adjuvant in the treatment of rheumatoid arthritis.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"137-145"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The hepatoprotective effects of sitagliptin against cyclophosphamide-induced hepatotoxicity in rat. 西他列汀对环磷酰胺诱导的大鼠肝毒性的保护作用
IF 1.5 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-01-01 DOI: 10.22099/mbrc.2024.49925.1964
Reza Maleki, Mohammad Foad Noorbakhsh, Nasrin Kazemipour, Maliheh Masoudian, Fatemeh Namazi, Saeed Nazifi

Hepatotoxicity is a serious side effects of cyclophosphamide. Thus, the present research investigates the protective properties of sitagliptin against cyclophosphamide-induced hepatotoxicity. Fifty male rats were randomly divided into five groups. They were pre-treated with either sitagliptin or normal saline once a day for the first ten days of the study. To induce acute hepatotoxicity, cyclophosphamide (200 mg/kg, i.p) was injected only one time and 45 min after the last dose of sitagliptin. The rats were sacrificed on the 11th day, and their blood and liver were collected for biochemical, gene expression, and histopathological assessments. Our results showed that cyclophosphamide induced obvious liver toxicity as marked by an increase in serum levels of alanine transaminase and aspartate transaminase, reduced serum albumin and total protein levels, in addition to histopathological changes. The malondialdehyde, tumor necrosis factor-α, and interleukin-6 levels were also elevated and total antioxidant capacity declined in serum and hepatic homogenates. Sitagliptin magnificently attenuated the cylophosphamide-induced histological alterations, improved liver function tests, enhanced total antioxidant capacity, and decreased malondialdehyde, tumor necrosis factor-α, and interleukin-6 in the blood and hepatic tissues. These findings suggest that sitagliptin has hepatoprotective activity against cyclophosphamide toxicity, which may be due to its antioxidant and anti-inflammatory effects.

肝毒性是环磷酰胺的一种严重副作用。因此,本研究探讨了西他列汀对环磷酰胺引起的肝毒性的保护作用。50 只雄性大鼠被随机分为五组。在研究的前十天,它们每天接受一次西他列汀或生理盐水的预处理。为了诱导急性肝毒性,在最后一次服用西格列汀后 45 分钟,只注射一次环磷酰胺(200 毫克/千克,静脉注射)。大鼠在第 11 天被处死,收集其血液和肝脏进行生化、基因表达和组织病理学评估。结果表明,环磷酰胺会引起明显的肝脏毒性,表现为血清中丙氨酸转氨酶和天门冬氨酸转氨酶水平升高,血清白蛋白和总蛋白水平降低,以及组织病理学变化。血清和肝匀浆中的丙二醛、肿瘤坏死因子-α和白细胞介素-6水平也升高,总抗氧化能力下降。西他列汀大大减轻了环磷酰胺诱导的组织学改变,改善了肝功能测试,提高了总抗氧化能力,降低了血液和肝组织中的丙二醛、肿瘤坏死因子-α和白细胞介素-6。这些研究结果表明,西他列汀具有抗环磷酰胺毒性的保肝活性,这可能是由于它的抗氧化和抗炎作用。
{"title":"The hepatoprotective effects of sitagliptin against cyclophosphamide-induced hepatotoxicity in rat.","authors":"Reza Maleki, Mohammad Foad Noorbakhsh, Nasrin Kazemipour, Maliheh Masoudian, Fatemeh Namazi, Saeed Nazifi","doi":"10.22099/mbrc.2024.49925.1964","DOIUrl":"10.22099/mbrc.2024.49925.1964","url":null,"abstract":"<p><p>Hepatotoxicity is a serious side effects of cyclophosphamide. Thus, the present research investigates the protective properties of sitagliptin against cyclophosphamide-induced hepatotoxicity. Fifty male rats were randomly divided into five groups. They were pre-treated with either sitagliptin or normal saline once a day for the first ten days of the study. To induce acute hepatotoxicity, cyclophosphamide (200 mg/kg, i.p) was injected only one time and 45 min after the last dose of sitagliptin. The rats were sacrificed on the 11th day, and their blood and liver were collected for biochemical, gene expression, and histopathological assessments. Our results showed that cyclophosphamide induced obvious liver toxicity as marked by an increase in serum levels of alanine transaminase and aspartate transaminase, reduced serum albumin and total protein levels, in addition to histopathological changes. The malondialdehyde, tumor necrosis factor-α, and interleukin-6 levels were also elevated and total antioxidant capacity declined in serum and hepatic homogenates. Sitagliptin magnificently attenuated the cylophosphamide-induced histological alterations, improved liver function tests, enhanced total antioxidant capacity, and decreased malondialdehyde, tumor necrosis factor-α, and interleukin-6 in the blood and hepatic tissues. These findings suggest that sitagliptin has hepatoprotective activity against cyclophosphamide toxicity, which may be due to its antioxidant and anti-inflammatory effects.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 4","pages":"193-200"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Molecular Biology Research Communications
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1