Mehdi Rostami, Seyed Amir Vaezzade, Elaheh Gheybi, Hanieh Nadi Azadi, Arezoo Rajabian, Fatemeh Forouzanfar, Mohammad Soukhtanloo
Objectives: An abnormal buildup of Quinolinic Acid (QuA) is usually linked to the death of nerve cells and a condition known as neuritis in various forms of neurodegenerative illness. Alpha Lipoic Acid (ALA) has substantial antioxidant properties, according to previous studies. However, the protective effects of ALA against the neurotoxicity induced by QuA are unknown. This work aimed to determine whether ALA could shield the SH-SY5Y neuroblastoma cell line from QuA-induced neurotoxicity. Methods: Cell viability was assessed using the MTT assay, while cell cycle and apoptotic effects were evaluated using flow cytometry. Cellular levels of reactive oxygen species (ROS) were also examined. Results: The findings showed that ALA, at non-toxic concentrations, had a protective effect against QuA-induced toxicity. Moreover, pretreatment with ALA reduced the number of cells that underwent apoptosis. Also, it was found that the percentage of apoptotic cells (i.e., those in the sub-G1 phase) was considerably increased following QuA therapy. ALA also dramatically reduced the production of ROS by QuA. Conclusion: The results suggest that ALA appears to be an effective neuroprotectant and antioxidant against QuA-induced neurotoxicity.
目的：喹啉酸（Quinolinic Acid，QuA）的异常积聚通常与神经细胞的死亡和各种神经退行性疾病中的神经炎有关。根据以往的研究，α-硫辛酸（ALA）具有很强的抗氧化性。然而，ALA 对 QuA 引起的神经毒性的保护作用尚不清楚。本研究旨在确定 ALA 能否保护 SH-SY5Y 神经母细胞瘤细胞系免受 QuA 诱导的神经毒性的影响。方法：使用 MTT 检测法评估细胞活力，同时使用流式细胞术评估细胞周期和凋亡效应。还检测了细胞中活性氧（ROS）的水平。结果：研究结果表明，无毒浓度的 ALA 对 QuA 诱导的毒性有保护作用。此外，用 ALA 预处理可减少细胞凋亡的数量。研究还发现，QuA 治疗后，凋亡细胞（即处于亚 G1 期的细胞）的比例显著增加。ALA 还能显著减少 QuA 产生的 ROS。结论研究结果表明，ALA 似乎是一种有效的神经保护剂和抗氧化剂，可预防 QuA 引起的神经毒性。
{"title":"Alpha Lipoic Acid Protects Human SH-SY5Y Cells Against Quinolinic Acid-Induced Toxicity: Focusing on ROS Levels and Cell Cycle","authors":"Mehdi Rostami, Seyed Amir Vaezzade, Elaheh Gheybi, Hanieh Nadi Azadi, Arezoo Rajabian, Fatemeh Forouzanfar, Mohammad Soukhtanloo","doi":"10.18502/abi.v1i4.14723","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14723","url":null,"abstract":"Objectives: An abnormal buildup of Quinolinic Acid (QuA) is usually linked to the death of nerve cells and a condition known as neuritis in various forms of neurodegenerative illness. Alpha Lipoic Acid (ALA) has substantial antioxidant properties, according to previous studies. However, the protective effects of ALA against the neurotoxicity induced by QuA are unknown. This work aimed to determine whether ALA could shield the SH-SY5Y neuroblastoma cell line from QuA-induced neurotoxicity. \u0000Methods: Cell viability was assessed using the MTT assay, while cell cycle and apoptotic effects were evaluated using flow cytometry. Cellular levels of reactive oxygen species (ROS) were also examined. \u0000Results: The findings showed that ALA, at non-toxic concentrations, had a protective effect against QuA-induced toxicity. Moreover, pretreatment with ALA reduced the number of cells that underwent apoptosis. Also, it was found that the percentage of apoptotic cells (i.e., those in the sub-G1 phase) was considerably increased following QuA therapy. ALA also dramatically reduced the production of ROS by QuA. \u0000Conclusion: The results suggest that ALA appears to be an effective neuroprotectant and antioxidant against QuA-induced neurotoxicity.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"12 23","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139523582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Rostami, Asghar Beiranvand, Sarmad Nourooz-Zadeh, Massoumeh Rostami, Afshin Mohammadi, J. Nourooz-Zadeh
Objectives: Thyroid Ultrasonography (US) is recommended as a valuable tool for evaluating the status and function of the thyroid gland. The objective of this study was to compare and analyze the thyroid ultrasonography outcomes in children and adolescents who have normal thyroid function and thyroid antibodies. Methods: A cross-sectional study was conducted on a group of 233 selected females aged 9 to 14 years old. Blood samples were obtained from the subjects and analyzed for thyroid hormones and thyroid autoantibodies. Additionally, a thyroid ultrasound was performed to provide an in-depth evaluation. Results: Of all the participants, 25% displayed hypoechogenicity. Individuals with reduced echogenicity had higher median levels of thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (TPO-Ab), and thyroglobulin antibody (Tg-Ab) compared to those with normal echogenicity. Moreover, those with hypoechogenicity had significantly higher thyroid volume (TVol), iodine status, and thyroglobulin levels than their counterparts with normal echogenicity. Hypoechogenicity was also significantly associated with higher levels of TPO-Ab, Tg-Ab, and TSH. Logistic regression analysis revealed that high TSH and TPO-Ab levels were associated with a higher risk of irregular echo patterns and thyroid autoantibodies. Conclusion: The results revealed that irregular thyroid patterns in the ultrasonography were useful for assessing thyroid structure and dysfunction. Moreover, elevated TPOAb, Tg-Ab, and TSH concentrations in the serum may indicate thyroid malfunction. Ultrasound can help to identify early thyroid dysfunction along with the standard thyroid assessment biomarkers.
{"title":"Association between Thyroid Function indices and Thyroid Autoantibodies with Thyroid Ultrasonography Outcomes in Children and Adolescents","authors":"R. Rostami, Asghar Beiranvand, Sarmad Nourooz-Zadeh, Massoumeh Rostami, Afshin Mohammadi, J. Nourooz-Zadeh","doi":"10.18502/abi.v1i4.14721","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14721","url":null,"abstract":"Objectives: Thyroid Ultrasonography (US) is recommended as a valuable tool for evaluating the status and function of the thyroid gland. The objective of this study was to compare and analyze the thyroid ultrasonography outcomes in children and adolescents who have normal thyroid function and thyroid antibodies. \u0000Methods: A cross-sectional study was conducted on a group of 233 selected females aged 9 to 14 years old. Blood samples were obtained from the subjects and analyzed for thyroid hormones and thyroid autoantibodies. Additionally, a thyroid ultrasound was performed to provide an in-depth evaluation. \u0000Results: Of all the participants, 25% displayed hypoechogenicity. Individuals with reduced echogenicity had higher median levels of thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (TPO-Ab), and thyroglobulin antibody (Tg-Ab) compared to those with normal echogenicity. Moreover, those with hypoechogenicity had significantly higher thyroid volume (TVol), iodine status, and thyroglobulin levels than their counterparts with normal echogenicity. Hypoechogenicity was also significantly associated with higher levels of TPO-Ab, Tg-Ab, and TSH. Logistic regression analysis revealed that high TSH and TPO-Ab levels were associated with a higher risk of irregular echo patterns and thyroid autoantibodies. \u0000Conclusion: The results revealed that irregular thyroid patterns in the ultrasonography were useful for assessing thyroid structure and dysfunction. Moreover, elevated TPOAb, Tg-Ab, and TSH concentrations in the serum may indicate thyroid malfunction. Ultrasound can help to identify early thyroid dysfunction along with the standard thyroid assessment biomarkers.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Negar Dinarvand, Mojdeh Rahimi, H. Shahbazian, M. Birgani, Bahman Cheraghian, Narges Mohammadtaghvaei
Objectives: The proprotein convertase subtilisin/kexin type 7 (PCSK7) enzyme is encoded by the PCSK7 gene and is involved in the processing and activation of latent precursor proteins. Previous studies have reported that some PCSK7 variants are associated with markers of body iron stores and lipid profiles, as well as obesity and insulin resistance. The aim of this study was to investigate the association of the rs236918 variant of PCSK7 with metabolic syndrome (MetS) and its related components. Methods: In this cross-sectional study, 325 participants in the age group of 25 to 86 years were examined. Standard protocols were employed to measure body mass index, blood pressure, fasting blood glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Individuals with metabolic syndrome (MetS) were identified in accordance with the guidelines set by the National Cholesterol Education Program. Genotype was determined using the PCR-RFLP method. Results: The findings revealed that there was no association between the rs236918 variant and increased risk of MetS or its components and also plasma lipid profile. Conclusion: Overall, the findings exhibit no significant association between the PCSK7 rs236918 polymorphism and MetS in this population. Although these results may be due to sample size and power issues, the role of lifestyle factors and other genes in the development of MetS appears to be more important in this population. Therefore, further research is required to validate these results.
{"title":"Association of the rs236918 variant of PCSK7 with the prevalence of the metabolic syndrome and its components in population from Ahvaz cohort study: A case-control study in Iran","authors":"Negar Dinarvand, Mojdeh Rahimi, H. Shahbazian, M. Birgani, Bahman Cheraghian, Narges Mohammadtaghvaei","doi":"10.18502/abi.v1i4.14722","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14722","url":null,"abstract":"Objectives: The proprotein convertase subtilisin/kexin type 7 (PCSK7) enzyme is encoded by the PCSK7 gene and is involved in the processing and activation of latent precursor proteins. Previous studies have reported that some PCSK7 variants are associated with markers of body iron stores and lipid profiles, as well as obesity and insulin resistance. The aim of this study was to investigate the association of the rs236918 variant of PCSK7 with metabolic syndrome (MetS) and its related components. \u0000Methods: In this cross-sectional study, 325 participants in the age group of 25 to 86 years were examined. Standard protocols were employed to measure body mass index, blood pressure, fasting blood glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG). Individuals with metabolic syndrome (MetS) were identified in accordance with the guidelines set by the National Cholesterol Education Program. Genotype was determined using the PCR-RFLP method. \u0000Results: The findings revealed that there was no association between the rs236918 variant and increased risk of MetS or its components and also plasma lipid profile. \u0000Conclusion: Overall, the findings exhibit no significant association between the PCSK7 rs236918 polymorphism and MetS in this population. Although these results may be due to sample size and power issues, the role of lifestyle factors and other genes in the development of MetS appears to be more important in this population. Therefore, further research is required to validate these results.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"6 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Amirhossein Sangdari, Amir Karbalaee-Hasani, Mojtaba Fathi, Hadi Khodabandehloo
Objectives: Advanced glycation end products (AGEs) play an important role in the development and progression of diabetic complications. The receptor for AGE (RAGE) is the ligand-binding site of AGE that initiates and accelerates the atherosclerotic process. Plasminogen activator inhibitor-1 (PAI-1) is a prothrombotic factor that has been proposed as a biological marker for prognostic assessment, monitoring of microvascular and macrovascular complications in diabetes. The purpose of this study is to investigate the effects of aminoguanidine on RAGE and PAI-1 expression levels in the liver of streptozotocin-induced diabetic rats. Methods: Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ, 50 mg/kg). On day 3, diabetic rats were administered 50, 100, and 200 mg/kg/day of aminoguanidine. The expression of PAI-1 and RAGE in the liver tissue was evaluated using real-time PCR. Results: PAI-1 and RAGE gene expression levels were higher in the liver of the diabetic rats compared to the control group. Aminoguanidine at 50, 100, and 200 mg/kg decreased PAI-1 and RAGE gene expression in the liver (p<0.001 at all doses). However, these genes were downregulated only at a dose of 200 mg/kg in healthy rats (p<0.0001). In addition, hepatic AGE protein levels were significantly decreased following treatment of the diabetic rats with aminoguanidine (p<0.001). There was also a significant correlation between AGE protein concentration and the expression of PAI-1 and RAGE. Conclusion: In summary, the data of the present study suggest that aminoguanidine reduced the expression of PAI-1 and RAGE in the liver of the diabetic rats.
{"title":"Effect of aminoguanidine on plasminogen activator inhibitor-1 and receptor of advanced glycation endproduct in the liver of streptozotocin-induced diabetic rats","authors":"Amirhossein Sangdari, Amir Karbalaee-Hasani, Mojtaba Fathi, Hadi Khodabandehloo","doi":"10.18502/abi.v1i4.14720","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14720","url":null,"abstract":"Objectives: Advanced glycation end products (AGEs) play an important role in the development and progression of diabetic complications. The receptor for AGE (RAGE) is the ligand-binding site of AGE that initiates and accelerates the atherosclerotic process. Plasminogen activator inhibitor-1 (PAI-1) is a prothrombotic factor that has been proposed as a biological marker for prognostic assessment, monitoring of microvascular and macrovascular complications in diabetes. The purpose of this study is to investigate the effects of aminoguanidine on RAGE and PAI-1 expression levels in the liver of streptozotocin-induced diabetic rats. \u0000Methods: Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ, 50 mg/kg). On day 3, diabetic rats were administered 50, 100, and 200 mg/kg/day of aminoguanidine. The expression of PAI-1 and RAGE in the liver tissue was evaluated using real-time PCR. \u0000Results: PAI-1 and RAGE gene expression levels were higher in the liver of the diabetic rats compared to the control group. Aminoguanidine at 50, 100, and 200 mg/kg decreased PAI-1 and RAGE gene expression in the liver (p<0.001 at all doses). However, these genes were downregulated only at a dose of 200 mg/kg in healthy rats (p<0.0001). In addition, hepatic AGE protein levels were significantly decreased following treatment of the diabetic rats with aminoguanidine (p<0.001). There was also a significant correlation between AGE protein concentration and the expression of PAI-1 and RAGE. \u0000Conclusion: In summary, the data of the present study suggest that aminoguanidine reduced the expression of PAI-1 and RAGE in the liver of the diabetic rats.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"5 16","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tahmineh Ostovar, G. Goodarzi, S. Samavarchi Tehrani
The newest class of noncoding RNAs with distinctive characteristics is called circular RNAs (circRNAs). These novel RNAs are more stable than other RNAs because they lack 5’ and 3’ ends, instead having their two ends created from pre-mRNA through a process called back-splicing. They are also widely expressed in a variety of species, including viruses, plants, and mammals. There is growing evidence that circRNAs are enriched in the NF-κB pathway. The development of many types of malignancies is associated with aberrant activation of the NF-κB pathway. Recent findings indicate that the circRNA/NF-κB axis controls the expression of genes linked to cancer and, consequently, the growth of tumors. Moreover, circRNAs might interact with the NF-κB pathway to affect biological processes of cells. A comprehensive understanding of the molecular processes behind the involvement of circRNA linked to the NF-κB pathway in the progression of distinct malignancies would provide novel opportunities for cancer therapy. Therefore, this article will briefly discuss the function of circRNAs and the NFκB pathway in cancer. Next, it will address the crucial role that circRNAs associated with NF-κB play in the progression of different types of malignancies.
{"title":"Modulation of cancer progression by circRNA/ NF-kB axis","authors":"Tahmineh Ostovar, G. Goodarzi, S. Samavarchi Tehrani","doi":"10.18502/abi.v1i4.14717","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14717","url":null,"abstract":"The newest class of noncoding RNAs with distinctive characteristics is called circular RNAs (circRNAs). These novel RNAs are more stable than other RNAs because they lack 5’ and 3’ ends, instead having their two ends created from pre-mRNA through a process called back-splicing. They are also widely expressed in a variety of species, including viruses, plants, and mammals. There is growing evidence that circRNAs are enriched in the NF-κB pathway. The development of many types of malignancies is associated with aberrant activation of the NF-κB pathway. Recent findings indicate that the circRNA/NF-κB axis controls the expression of genes linked to cancer and, consequently, the growth of tumors. Moreover, circRNAs might interact with the NF-κB pathway to affect biological processes of cells. A comprehensive understanding of the molecular processes behind the involvement of circRNA linked to the NF-κB pathway in the progression of distinct malignancies would provide novel opportunities for cancer therapy. Therefore, this article will briefly discuss the function of circRNAs and the NFκB pathway in cancer. Next, it will address the crucial role that circRNAs associated with NF-κB play in the progression of different types of malignancies.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"10 24","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ali Karami Robati, Zahra Shahsavari, Mohammad Amin Vaezi, Banafsheh Safizadeh, Farzad Izak Shirian, Masoumeh Tavakoli-Yaraki
Objectives: The aim of this study is to evaluate the potential effect of caffeic acid (CAF) on the growth of breast cancer cells, in addition to determining the contributing role of caspases, mitochondria, and oxidative status. Methods: MCF-7 and MDA-MB-468 breast cancer cells were exposed to varying concentrations of CAF for different periods of time. The potential cytotoxic effect was measured using the MTT assay. The activities of caspase 3 and caspase 8, as well as the cellular level of reactive oxygen species (ROS) and the level of mitochondrial membrane potential (Δψm), were evaluated in different groups of cells. Results: The findings showed that CAF decreased the percentage of MCF-7 and MDAMB-468 cells in a manner that depended on the dose and duration of exposure. The death of breast cancer cells induced by CAF was associated with an increase in ROS level in both cell lines. The decrease in mitochondrial membrane potential (Δψm) following CAF treatment suggests that mitochondrial dysfunction may be involved in the death of breast cancer cells induced by CAF. Importantly, the activity of caspase 8 increased after treatment, indicating the potential involvement of the extrinsic apoptosis pathway in the inhibition of breast cancer cell growth by CAF. The dosage of 20µm of CAF following 48 hours of incubation appeared to have the most significant impact on breast cancer cells. Conclusion: The study highlights the potential pro-apoptotic effect of CAF in both estrogen-positive and estrogen-negative breast cancer cells. This, in conjunction with other evidence, may lead to new insights for more effective therapeutic approaches in breast cancer
{"title":"Caffeic acid stimulates breast cancer death through Reactive oxygen species (ROS) formation, Caspase activation and mitochondrial membrane potential depletion","authors":"Ali Karami Robati, Zahra Shahsavari, Mohammad Amin Vaezi, Banafsheh Safizadeh, Farzad Izak Shirian, Masoumeh Tavakoli-Yaraki","doi":"10.18502/abi.v1i4.14719","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14719","url":null,"abstract":"Objectives: The aim of this study is to evaluate the potential effect of caffeic acid (CAF) on the growth of breast cancer cells, in addition to determining the contributing role of caspases, mitochondria, and oxidative status. \u0000Methods: MCF-7 and MDA-MB-468 breast cancer cells were exposed to varying concentrations of CAF for different periods of time. The potential cytotoxic effect was measured using the MTT assay. The activities of caspase 3 and caspase 8, as well as the cellular level of reactive oxygen species (ROS) and the level of mitochondrial membrane potential (Δψm), were evaluated in different groups of cells. \u0000Results: The findings showed that CAF decreased the percentage of MCF-7 and MDAMB-468 cells in a manner that depended on the dose and duration of exposure. The death of breast cancer cells induced by CAF was associated with an increase in ROS level in both cell lines. The decrease in mitochondrial membrane potential (Δψm) following CAF treatment suggests that mitochondrial dysfunction may be involved in the death of breast cancer cells induced by CAF. Importantly, the activity of caspase 8 increased after treatment, indicating the potential involvement of the extrinsic apoptosis pathway in the inhibition of breast cancer cell growth by CAF. The dosage of 20µm of CAF following 48 hours of incubation appeared to have the most significant impact on breast cancer cells. \u0000Conclusion: The study highlights the potential pro-apoptotic effect of CAF in both estrogen-positive and estrogen-negative breast cancer cells. This, in conjunction with other evidence, may lead to new insights for more effective therapeutic approaches in breast cancer","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"1 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mahdieh Aliyari, S. Hashemy, Farideh Ghavidel, Hossein Hosseini
Objectives: Type 2 diabetes has become a global health burden, especially in developing nations, and is frequently linked to dyslipidemia. While various medications are available, there is a growing interest in herbal remedies such as Nigella sativa (N. sativa) as alternative treatments for type 2 diabetes. In this systematic review and meta-analysis, the objective was to assess the impact of N. sativa on the lipid profile of patients with type 2 diabetes. Methods: Online databases, including Web of Science, Scopus, PubMed, and EMBASE, were searched. Changes in lipid profile parameters were reported as weighted mean differences, along with a 95% confidence interval. Sensitivity analysis, quality assessment, subgroup analysis, and publication bias were evaluated in the eligible studies. Results: The study was performed on eight randomized controlled trials (RCTs) involving 1030 participants. According to the findings, supplementation of N. sativa in the form of seed powder or oil significantly reduced total cholesterol and LDL-cholesterol levels, while increasing HDL-cholesterol levels in patients with type 2 diabetes. The funnel plot exhibited visual symmetry for the studies included in the meta-analysis. Conclusion: The findings indicate that N sativa may be beneficial as an adjunctive treatment alongside standard medications for managing dyslipidemia in individuals with type 2 diabetes.
目的：2 型糖尿病已成为全球健康负担，尤其是在发展中国家，而且经常与血脂异常有关。虽然有多种药物可供选择，但人们对将黑麦草（Nigella sativa）等草药作为 2 型糖尿病替代疗法的兴趣与日俱增。本系统综述和荟萃分析旨在评估 N. sativa 对 2 型糖尿病患者血脂状况的影响。研究方法搜索在线数据库，包括 Web of Science、Scopus、PubMed 和 EMBASE。血脂谱参数的变化以加权平均差和 95% 置信区间的形式进行报告。对符合条件的研究进行了敏感性分析、质量评估、亚组分析和发表偏倚评估。研究结果本研究对 8 项随机对照试验（RCT）进行了分析，共有 1030 人参与。研究结果表明，以种子粉或油的形式补充 N. sativa 能显著降低 2 型糖尿病患者的总胆固醇和低密度脂蛋白胆固醇水平，同时提高高密度脂蛋白胆固醇水平。纳入荟萃分析的研究的漏斗图显示出视觉对称性。结论研究结果表明，藜芦作为一种辅助治疗方法，可与标准药物一起用于控制 2 型糖尿病患者的血脂异常。
{"title":"Effect of Nigella sativa Supplementation on Lipid Profile in Type 2 Diabetes: A Systematic Review and Meta-analysis of Randomized Ccontrolled Trials","authors":"Mahdieh Aliyari, S. Hashemy, Farideh Ghavidel, Hossein Hosseini","doi":"10.18502/abi.v1i4.14718","DOIUrl":"https://doi.org/10.18502/abi.v1i4.14718","url":null,"abstract":"Objectives: Type 2 diabetes has become a global health burden, especially in developing nations, and is frequently linked to dyslipidemia. While various medications are available, there is a growing interest in herbal remedies such as Nigella sativa (N. sativa) as alternative treatments for type 2 diabetes. In this systematic review and meta-analysis, the objective was to assess the impact of N. sativa on the lipid profile of patients with type 2 diabetes. \u0000Methods: Online databases, including Web of Science, Scopus, PubMed, and EMBASE, were searched. Changes in lipid profile parameters were reported as weighted mean differences, along with a 95% confidence interval. Sensitivity analysis, quality assessment, subgroup analysis, and publication bias were evaluated in the eligible studies. \u0000Results: The study was performed on eight randomized controlled trials (RCTs) involving 1030 participants. According to the findings, supplementation of N. sativa in the form of seed powder or oil significantly reduced total cholesterol and LDL-cholesterol levels, while increasing HDL-cholesterol levels in patients with type 2 diabetes. The funnel plot exhibited visual symmetry for the studies included in the meta-analysis. \u0000Conclusion: The findings indicate that N sativa may be beneficial as an adjunctive treatment alongside standard medications for managing dyslipidemia in individuals with type 2 diabetes.","PeriodicalId":512811,"journal":{"name":"Acta Biochimica Iranica","volume":"9 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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