Qiang Sun, Jun Yao, Shuxun Wei, Xinxing Li, Weijun Wang
Since the symptoms of early gastric cancer patients are not obvious, the majority of new gastric cancer cases are progressive gastric cancer every year. In this paper, we applied nanomedicine technology to design and prepare multifunctional nanoparticles for the diagnosis and treatment of gastric cancer. Through targeted imaging of gastric cancer, combined with phototherapy and the prepared nanoprobes are applied to the ectopic transplantation tumor model of gastric cancer. Meanwhile, a fluorescent microsensor based on graphene oxide and deoxyribonuclease is constructed in order to realize the rapid detection of gastric cancer exosomes. The near-infrared multifunctional nanoprobe is combined with artificial intelligence microsensor technology and applied to the molecular diagnosis of gastric cancer. The results shows that the P-P-I-M+ laser irradiation group has the highest fluorescence intensity and its average fluorescence intensity is 2.04 times higher than that of the P-P-I+ laser irradiation group. The relative cell viability of P-P-M+ laser irradiation group, P-P-I+ laser irradiation group and P-P-I-M+ laser irradiation group are 62.5%, 41.9% and 19.3%, respectively. Therefore, the method in this paper can reduce the non-specific toxicity to other organs as well as exert the effect of combining the diagnosis and treatment of gastric cancer.
{"title":"The Value of Near-Infrared Multifunctional Nanoprobe Combined with Artificial Intelligence Microsensor Technology in Molecular Diagnosis for Gastric Cancer","authors":"Qiang Sun, Jun Yao, Shuxun Wei, Xinxing Li, Weijun Wang","doi":"10.1166/jbn.2024.3769","DOIUrl":"https://doi.org/10.1166/jbn.2024.3769","url":null,"abstract":"Since the symptoms of early gastric cancer patients are not obvious, the majority of new gastric cancer cases are progressive gastric cancer every year. In this paper, we applied nanomedicine technology to design and prepare multifunctional nanoparticles for the diagnosis and treatment\u0000 of gastric cancer. Through targeted imaging of gastric cancer, combined with phototherapy and the prepared nanoprobes are applied to the ectopic transplantation tumor model of gastric cancer. Meanwhile, a fluorescent microsensor based on graphene oxide and deoxyribonuclease is constructed\u0000 in order to realize the rapid detection of gastric cancer exosomes. The near-infrared multifunctional nanoprobe is combined with artificial intelligence microsensor technology and applied to the molecular diagnosis of gastric cancer. The results shows that the P-P-I-M+ laser irradiation group\u0000 has the highest fluorescence intensity and its average fluorescence intensity is 2.04 times higher than that of the P-P-I+ laser irradiation group. The relative cell viability of P-P-M+ laser irradiation group, P-P-I+ laser irradiation group and P-P-I-M+ laser irradiation group are 62.5%,\u0000 41.9% and 19.3%, respectively. Therefore, the method in this paper can reduce the non-specific toxicity to other organs as well as exert the effect of combining the diagnosis and treatment of gastric cancer.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139825069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A mouse renal ischemia-reperfusion injury (RIRI) model was used to investigate how follistatin-Like Protein 1 (FSTL1) provides renal protection post-RIRI by targeting inflammation, apoptosis, and microRNA (miRNA). RIRI was induced in 8-week-old male C57BL/6 mice, followed by FSTL1 recombinant protein treatment. Inflammation and apoptosis in kidney tissues were assessed using ELISA and flow cytometry. A cellular RIRI model was created using hypoxia/reoxygenation (H/R) in HK-2 cells to validate FSTL1’s effects. miRNA-mediated mechanisms were explored using cell transfection and dual-luciferase assays. RIRI mice exhibited elevated inflammation and apoptosis, while FSTL1 treatment mitigated these effects. Similarly, FSTL1 attenuated H/R-induced HK-2 cell damage. miR-21 expression decreased in H/R-treated HK-2 cells, which FSTL1 reversed. miR-21 mimic reduced H/R-induced HK-2 cell damage, while its inhibition decreased FSTL1’s protection. Notably, miR-21 targeted caspase-7 and suppressed its activity. FSTL1 alleviated mouse RIRI by upregulating miR-21, thereby reducing inflammation and apoptosis in kidney tissues post-RIRI. This study highlights FSTL1’s therapeutic potential through the miR-21-mediated regulation of inflammation and apoptosis in RIRI.
{"title":"Follistatin-Like Protein 1 Alleviates Renal Ischemia-Reperfusion Injury by Regulating MicroRNA-21","authors":"Guoxiong Lin, Shiquan Chai, Kaibo Mei, Guixiang Xiong, Fanglan Liu, Haifei Mao","doi":"10.1166/jbn.2024.3760","DOIUrl":"https://doi.org/10.1166/jbn.2024.3760","url":null,"abstract":"A mouse renal ischemia-reperfusion injury (RIRI) model was used to investigate how follistatin-Like Protein 1 (FSTL1) provides renal protection post-RIRI by targeting inflammation, apoptosis, and microRNA (miRNA). RIRI was induced in 8-week-old male C57BL/6 mice, followed by FSTL1 recombinant\u0000 protein treatment. Inflammation and apoptosis in kidney tissues were assessed using ELISA and flow cytometry. A cellular RIRI model was created using hypoxia/reoxygenation (H/R) in HK-2 cells to validate FSTL1’s effects. miRNA-mediated mechanisms were explored using cell transfection\u0000 and dual-luciferase assays. RIRI mice exhibited elevated inflammation and apoptosis, while FSTL1 treatment mitigated these effects. Similarly, FSTL1 attenuated H/R-induced HK-2 cell damage. miR-21 expression decreased in H/R-treated HK-2 cells, which FSTL1 reversed. miR-21 mimic reduced H/R-induced\u0000 HK-2 cell damage, while its inhibition decreased FSTL1’s protection. Notably, miR-21 targeted caspase-7 and suppressed its activity. FSTL1 alleviated mouse RIRI by upregulating miR-21, thereby reducing inflammation and apoptosis in kidney tissues post-RIRI. This study highlights FSTL1’s\u0000 therapeutic potential through the miR-21-mediated regulation of inflammation and apoptosis in RIRI.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139826206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paeoniflorin (PAE) is an active ingredient extracted from peony. This study aimed to explore the mechanism by which liposome nanoparticles loaded with PAE protect neuronal damage in Parkinson’s disease. Model group, PAE group, PAE-Lips group, PAE-Lips+miR-135a agonist group, PAE-Lips+miR-135a inhibitor group, PAE-Lips+BAY11-7085 group, PAE-Lips+SC75741 group were designed. PCR, learning and memory ability testing, pole climbing test, etc. were used to determine the mechanism of PAE-Lips on Parkinson’s disease and whether it exerts effects through regulating miR-135a. PAE-Lips were successfully constructed. PAE-Lips improved Parkinson’s disease in rats and had a certain connection with miR-135a. Up-regulating miR-135a inhibited NF-κB pathway to a certain extent and improved Parkinson’s disease. It helped protect neurons. Further verification using PAE-Lips+miR-135a agonists, SC75741, BAY11-7085, etc. showed that PAE-Lips upregulated the expression of miR-135 and inhibited NF-κB pathway, which has a good protective effect on neurons in Parkinson’s disease. PAE-Lips can promote miR-135a to inhibit the NF-κB pathway, thereby protecting neuronal damage in Parkinson’s disease. This study will provide a new idea for the prevention and treatment of Parkinson’s disease, clarify the impact of PAE-Lips, miR-135a, NF-κB, BAY11-7085 and SC75741 on Parkinson’s disease, and provide a basis for the combined use of these interventions. The possibility of treating Parkinson’s disease more effectively deserves further exploration and research and provides a theoretical basis for the development of related therapeutic drugs.
{"title":"Liposome Nanoparticles Loaded with Paeoniflorin Protect Neuronal Damage in Parkinson’s Disease by Regulating miR-135a","authors":"Pin Wang, Dongxia Xia, Yihe Wang, Yue Qu","doi":"10.1166/jbn.2024.3801","DOIUrl":"https://doi.org/10.1166/jbn.2024.3801","url":null,"abstract":"Paeoniflorin (PAE) is an active ingredient extracted from peony. This study aimed to explore the mechanism by which liposome nanoparticles loaded with PAE protect neuronal damage in Parkinson’s disease. Model group, PAE group, PAE-Lips group, PAE-Lips+miR-135a agonist group, PAE-Lips+miR-135a\u0000 inhibitor group, PAE-Lips+BAY11-7085 group, PAE-Lips+SC75741 group were designed. PCR, learning and memory ability testing, pole climbing test, etc. were used to determine the mechanism of PAE-Lips on Parkinson’s disease and whether it exerts effects through regulating miR-135a. PAE-Lips\u0000 were successfully constructed. PAE-Lips improved Parkinson’s disease in rats and had a certain connection with miR-135a. Up-regulating miR-135a inhibited NF-κB pathway to a certain extent and improved Parkinson’s disease. It helped protect neurons. Further verification\u0000 using PAE-Lips+miR-135a agonists, SC75741, BAY11-7085, etc. showed that PAE-Lips upregulated the expression of miR-135 and inhibited NF-κB pathway, which has a good protective effect on neurons in Parkinson’s disease. PAE-Lips can promote miR-135a to inhibit the NF-κB\u0000 pathway, thereby protecting neuronal damage in Parkinson’s disease. This study will provide a new idea for the prevention and treatment of Parkinson’s disease, clarify the impact of PAE-Lips, miR-135a, NF-κB, BAY11-7085 and SC75741 on Parkinson’s disease, and\u0000 provide a basis for the combined use of these interventions. The possibility of treating Parkinson’s disease more effectively deserves further exploration and research and provides a theoretical basis for the development of related therapeutic drugs.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139827609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guixia Sun, Xiaohan Yu, Yan Zhou, Qinxue Cao, Dongle Zhang
This study investigated the altered expression of ADAMTS13 (a metalloproteinase) in a rat model of preeclampsia (PE)-induced kidney injury, along with its connection to inflammatory cytokines. Sprague-Dawley rats were divided into PE and Control groups. PE group rats were induced with Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to simulate PE-induced kidney injury. Key indicators such as systolic and diastolic blood pressure and proteinuria were assessed to confirm PE model success. Kidney tissue changes were examined through histology and cell apoptosis, while ADAMTS13 expression was studied using Western blotting and qRT-PCR. Plasma ADAMTS13 levels were correlated with interleukin-6 (IL-6) and IL-8 cytokines in PE rats. Elevated SBP, DBP, and proteinuria were evident in L-NAME-treated pregnant rats. Microscopic examination revealed glomerulocystic changes, thickened basement membranes, and increased apoptotic cells. Compared to Controls, PE rats exhibited decreased ADAMTS13 expression in renal tissues and plasma. Plasma IL-6 and IL-8 levels were elevated, inversely proportional to ADAMTS13 concentration in PE rats. In conclusion, PE-induced kidney injury reduced ADAMTS13 levels, correlating with heightened IL-6 and IL-8 concentrations, suggesting an interplay between ADAMTS13 and inflammatory cytokines.
本研究调查了子痫前期（PE）诱发肾损伤的大鼠模型中 ADAMTS13（一种金属蛋白酶）的表达变化及其与炎症细胞因子的关系。Sprague-Dawley 大鼠分为 PE 组和对照组。用 Nω-硝基-L-精氨酸甲酯盐酸盐（L-NAME）诱导 PE 组大鼠模拟 PE 诱导的肾损伤。对收缩压、舒张压和蛋白尿等主要指标进行评估，以确认 PE 模型是否成功。通过组织学和细胞凋亡检查肾组织的变化，同时使用 Western 印迹和 qRT-PCR 研究 ADAMTS13 的表达。PE 大鼠血浆 ADAMTS13 水平与白细胞介素-6（IL-6）和 IL-8 细胞因子相关。经 L-NAME 处理的妊娠大鼠明显出现 SBP、DBP 升高和蛋白尿。显微镜检查显示肾小球囊性变化、基底膜增厚和凋亡细胞增多。与对照组相比，PE 大鼠肾组织和血浆中的 ADAMTS13 表达减少。PE大鼠血浆中IL-6和IL-8水平升高，与ADAMTS13浓度成反比。总之，PE 引起的肾损伤降低了 ADAMTS13 的水平，与 IL-6 和 IL-8 浓度的升高相关，这表明 ADAMTS13 与炎症细胞因子之间存在相互作用。
{"title":"Correlations of ADAMTS13 Expression with Kidney Injury and Inflammatory Cytokine Changes in Rats with Preeclampsia","authors":"Guixia Sun, Xiaohan Yu, Yan Zhou, Qinxue Cao, Dongle Zhang","doi":"10.1166/jbn.2024.3759","DOIUrl":"https://doi.org/10.1166/jbn.2024.3759","url":null,"abstract":"This study investigated the altered expression of ADAMTS13 (a metalloproteinase) in a rat model of preeclampsia (PE)-induced kidney injury, along with its connection to inflammatory cytokines. Sprague-Dawley rats were divided into PE and Control groups. PE group rats were induced with\u0000 Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) to simulate PE-induced kidney injury. Key indicators such as systolic and diastolic blood pressure and proteinuria were assessed to confirm PE model success. Kidney tissue changes were examined through histology and cell\u0000 apoptosis, while ADAMTS13 expression was studied using Western blotting and qRT-PCR. Plasma ADAMTS13 levels were correlated with interleukin-6 (IL-6) and IL-8 cytokines in PE rats. Elevated SBP, DBP, and proteinuria were evident in L-NAME-treated pregnant rats. Microscopic examination revealed\u0000 glomerulocystic changes, thickened basement membranes, and increased apoptotic cells. Compared to Controls, PE rats exhibited decreased ADAMTS13 expression in renal tissues and plasma. Plasma IL-6 and IL-8 levels were elevated, inversely proportional to ADAMTS13 concentration in PE rats. In\u0000 conclusion, PE-induced kidney injury reduced ADAMTS13 levels, correlating with heightened IL-6 and IL-8 concentrations, suggesting an interplay between ADAMTS13 and inflammatory cytokines.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139830913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ziming Tan, Jun Wang, Mei Zhang, Hongtao Zhu, Qiong Luo
Central nervous system (CNS) inflammatory demyelinating diseases target oligodendrocytes or supporting cells. Millions of patients worldwide suffer from a variety of symptoms including vision. Motor and sensory impairments are increasingly recognized in children, but treatments for these disorders remain very limited. This study intends to assess the mechanism of miR-223 in inhibiting regulatory T cells differentiation in autoimmune encephalomyelitis. Electron microscopy revealed nanoparticle size. miR-223 expression in tissues was detected by mRNA. MTT method and flow cytometry were used to detect Treg cell activity, proliferation and differentiation. We further studied the mechanism by which miR-223 inhibits Treg differentiation and experimental autoimmune encephalomyelitis by targeting FOXO3-FOXP3. Animal experiments were conducted on the therapeutic potential of miR-223 antagonists to confirm whether miR-223 antagonists have an effect on Experimental allergic encephalomyelitis (EAE). In our previous studies, we found that the expression of miR-223 was up-regulated in EAE and children with MOG antibody-related demyelinating diseases. Through bioinformatics analysis, we found that FOXO3 could be used as a target gene of miR-223. FOXO3 is targeted by miR-223. Using nano-albumin particles as the carrier, miR-223 mimic reduced cell activity while FOXP3 overexpression partially offset the inhibitory effect. Overexpression of FOXP3 restored the Treg induced by using nano-albumin particles as the carrier of miR-223 mimic. Our study shows that nano-albumin particles carrying miR-223 can inhibit Treg cell differentiation by targeting FOXO3. This study provides a theoretical basis for clinical research.
{"title":"The Mechanism of miR-223 Inhibiting Treg Differentiation in Autoimmune Encephalomyelitis by Targeting Forkhead box-O3-Forkhead box-P3 Using Nano-Albumin Particles as a Carrier","authors":"Ziming Tan, Jun Wang, Mei Zhang, Hongtao Zhu, Qiong Luo","doi":"10.1166/jbn.2024.3793","DOIUrl":"https://doi.org/10.1166/jbn.2024.3793","url":null,"abstract":"Central nervous system (CNS) inflammatory demyelinating diseases target oligodendrocytes or supporting cells. Millions of patients worldwide suffer from a variety of symptoms including vision. Motor and sensory impairments are increasingly recognized in children, but treatments for\u0000 these disorders remain very limited. This study intends to assess the mechanism of miR-223 in inhibiting regulatory T cells differentiation in autoimmune encephalomyelitis. Electron microscopy revealed nanoparticle size. miR-223 expression in tissues was detected by mRNA. MTT method and flow\u0000 cytometry were used to detect Treg cell activity, proliferation and differentiation. We further studied the mechanism by which miR-223 inhibits Treg differentiation and experimental autoimmune encephalomyelitis by targeting FOXO3-FOXP3. Animal experiments were conducted on the therapeutic\u0000 potential of miR-223 antagonists to confirm whether miR-223 antagonists have an effect on Experimental allergic encephalomyelitis (EAE). In our previous studies, we found that the expression of miR-223 was up-regulated in EAE and children with MOG antibody-related demyelinating diseases. Through\u0000 bioinformatics analysis, we found that FOXO3 could be used as a target gene of miR-223. FOXO3 is targeted by miR-223. Using nano-albumin particles as the carrier, miR-223 mimic reduced cell activity while FOXP3 overexpression partially offset the inhibitory effect. Overexpression of FOXP3\u0000 restored the Treg induced by using nano-albumin particles as the carrier of miR-223 mimic. Our study shows that nano-albumin particles carrying miR-223 can inhibit Treg cell differentiation by targeting FOXO3. This study provides a theoretical basis for clinical research.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139882381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenfeng Liu, Meng Zhang, Xiaojie Du, Min Zhang, Weiling Wang, Zhiying Zhang
As a malignant tumor, cervical cancer (CC) seriously affects women’s life and health. Various microRNAs (miRNAs) are involved in tumorigenesis of CC. Here, we mainly paid attention to the effect of miR-153 in CC. RT-qPCR or Western blot was employed to quantify miR-153 or SATB1 expression. Molecular mechanism of miR-153/SATB1 was detected by Transwell and dual-luciferase assays. MiR-153 was downregulated in CC. Furthermore, upregulation of miR-153 restrained cell metastasis. Upregulation of SATB1 was detected in CC, and negative connected with miR-153 in CC cells. Knockdown of SATB1 suppressed cell metastasis in CC. The inhibitory effect of miR-153 was abolished by upregulation of SATB1. Besides that, miR-153 blocked EMT and downregulated p-β-catenin expression in CC cells. MiR-153 restrains cell metastasis and EMT in CC by targeting SATB1 and regulating Wnt/β-catenin pathway.
宫颈癌（CC）作为一种恶性肿瘤，严重影响着女性的生活和健康。多种微RNA（miRNA）参与了CC的肿瘤发生。在此，我们主要关注 miR-153 在 CC 中的作用。采用RT-qPCR或Western blot定量检测miR-153或SATB1的表达。通过Transwell和双荧光素酶实验检测了miR-153/SATB1的分子机制。CC中的miR-153被下调。此外，miR-153 的上调抑制了细胞的转移。在 CC 中检测到 SATB1 的上调，并且在 CC 细胞中与 miR-153 呈负相关。敲除SATB1抑制了CC细胞的转移。SATB1的上调会取消miR-153的抑制作用。此外，miR-153还能阻止EMT，并下调CC细胞中p-β-catenin的表达。MiR-153通过靶向SATB1和调节Wnt/β-catenin通路抑制CC细胞的转移和EMT。
{"title":"MicroRNA-153 Restrains Cell Metastasis and Epithelial–Mesenchymal Transition in Cervical Carcinoma by Targeting SATB1 and Regulating Wnt/β-Catenin Pathway","authors":"Wenfeng Liu, Meng Zhang, Xiaojie Du, Min Zhang, Weiling Wang, Zhiying Zhang","doi":"10.1166/jbn.2024.3761","DOIUrl":"https://doi.org/10.1166/jbn.2024.3761","url":null,"abstract":"As a malignant tumor, cervical cancer (CC) seriously affects women’s life and health. Various microRNAs (miRNAs) are involved in tumorigenesis of CC. Here, we mainly paid attention to the effect of miR-153 in CC. RT-qPCR or Western blot was employed to quantify miR-153 or SATB1\u0000 expression. Molecular mechanism of miR-153/SATB1 was detected by Transwell and dual-luciferase assays. MiR-153 was downregulated in CC. Furthermore, upregulation of miR-153 restrained cell metastasis. Upregulation of SATB1 was detected in CC, and negative connected with miR-153 in CC cells.\u0000 Knockdown of SATB1 suppressed cell metastasis in CC. The inhibitory effect of miR-153 was abolished by upregulation of SATB1. Besides that, miR-153 blocked EMT and downregulated p-β-catenin expression in CC cells. MiR-153 restrains cell metastasis and EMT in CC by targeting SATB1\u0000 and regulating Wnt/β-catenin pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139884054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yang Zhang, Jianglun Shen, Ning Li, Fen Hu, Faming Tian, Yiming Yang, Jinyin Yan, Haifeng Cai
This study assessed the mechanism of miR-21 with lipid nanoparticles carrier in restraining biological behavior of breast carcinoma cells through targeting of Wnt/β-catenin channel. Breast carcinoma cells were collected and divided into blank set, miR-21 set, agonist set and inhibitor set. We observed expressions of miR-21 cyclinD1, Bcl-2, Bax and Caspases-3. Also, quantity of cells through basement membrane, expression of factors related with Wnt/β-catenin signal channel, and targeting correlation between miR-21 and Wnt were also observed. The expression of miR-21 in MCF-7 cells was lowest, while the ratio of active cells in blank set was highest. The expressions of Bax and Caspase-3 and quantity of cells through basement membrane in the blank and agonist sets were highest. The expressions of cyclinD1 and Bcl-2 were lowest. The apoptotic rate in the blank and agonist sets was lowest and invasive rate was highest. The expressions of Wnt and β-catenin in the blank and agonist sets were highest. There was direct targeting correlation between miR-21 and Wnt while Wnt/β-catenin activity was restrained by miR-21. The expressions of Bax and Caspase-3 also increased and apoptosis was induced and invasion and proliferation of breast carcinoma cells were restrained.
{"title":"Mechanism of miR-21 Lipid Nanoparticles Carrier in Restraining Biological Behavior in Breast Carcinoma Through Targeting of Wnt/β-Catenin Channel","authors":"Yang Zhang, Jianglun Shen, Ning Li, Fen Hu, Faming Tian, Yiming Yang, Jinyin Yan, Haifeng Cai","doi":"10.1166/jbn.2024.3779","DOIUrl":"https://doi.org/10.1166/jbn.2024.3779","url":null,"abstract":"This study assessed the mechanism of miR-21 with lipid nanoparticles carrier in restraining biological behavior of breast carcinoma cells through targeting of Wnt/β-catenin channel. Breast carcinoma cells were collected and divided into blank set, miR-21 set, agonist set\u0000 and inhibitor set. We observed expressions of miR-21 cyclinD1, Bcl-2, Bax and Caspases-3. Also, quantity of cells through basement membrane, expression of factors related with Wnt/β-catenin signal channel, and targeting correlation between miR-21 and Wnt were also observed. The\u0000 expression of miR-21 in MCF-7 cells was lowest, while the ratio of active cells in blank set was highest. The expressions of Bax and Caspase-3 and quantity of cells through basement membrane in the blank and agonist sets were highest. The expressions of cyclinD1 and Bcl-2 were lowest. The\u0000 apoptotic rate in the blank and agonist sets was lowest and invasive rate was highest. The expressions of Wnt and β-catenin in the blank and agonist sets were highest. There was direct targeting correlation between miR-21 and Wnt while Wnt/β-catenin activity was restrained\u0000 by miR-21. The expressions of Bax and Caspase-3 also increased and apoptosis was induced and invasion and proliferation of breast carcinoma cells were restrained.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139878003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Libo Yuan, Ling Yao, Xianzhen Ren, Xusheng Chen, Kaiqiang Kang, Yongqing Xu, Tao Jin
Pyroptosis is a new type of cell death in the development of osteoarthritis (OA), but the underlying mechanism is not fully understood. This study aimed to investigate the role of Runx2 in the pyroptosis of chondrocyte (CH) and explore its effect on Caspase-1 expression. Human knee tissues from the fracture patients without OA history were collected. Human CHs isolated from the tissue were treated by lipopolysaccharide (LPS) to establish the model of OA. siRNA and CADD522 were used to block the function of Runx2. The cell viability was tested by MTT. The expression levels of Runx2, Caspase1/4/5/11, GSDMD, collagen-II, aggrecan, IL-1β, IL-8, and MMP3/9 were detected by RT-PCR, immunofluorescence, or western blot. Besides, the transcriptional association between Runx2 and Caspase-1 was confirmed by DNA immunoprecipitation and luciferase reporter assay. Runx2 and Caspase-1 expression were increased in LPS-treated CHs. Runx2 bound to the promoter of Caspase-1 and activated its expression. Moreover, silencing Runx2 or disrupting the DNA-binding ability of Runx2 attenuated the LPS-induced pyroptotic phenotype, containing Caspase-1 activation, collagen-II and aggrecan degradation, viability suppression, IL-1β and IL-8 upregulation. Blocking the expression or function of Runx2 alleviated the LPS-caused pyroptosis in CHs in the Caspase-1 manner, indicating a novel understanding of the pathology of OA.
热休克是骨关节炎（OA）发病过程中的一种新型细胞死亡方式，但其潜在机制尚未完全明了。本研究旨在研究Runx2在软骨细胞（CH）热噬中的作用，并探讨其对Caspase-1表达的影响。研究人员收集了无 OA 病史的骨折患者的人体膝关节组织。用 siRNA 和 CADD522 阻断 Runx2 的功能。用 MTT 检测细胞活力。通过 RT-PCR、免疫荧光或 Western blot 检测 Runx2、Caspase1/4/5/11、GSDMD、胶原蛋白-II、凝集素、IL-1β、IL-8 和 MMP3/9 的表达水平。此外，DNA免疫沉淀和荧光素酶报告实验也证实了Runx2和Caspase-1之间的转录关联。Runx2 和 Caspase-1 在 LPS 处理的 CHs 中表达增加。Runx2与Caspase-1的启动子结合并激活其表达。此外，沉默Runx2或破坏Runx2的DNA结合能力可减轻LPS诱导的嗜热表型，包括Caspase-1激活、胶原蛋白II和凝集素降解、活力抑制、IL-1β和IL-8上调。阻断Runx2的表达或功能能以Caspase-1的方式缓解LPS引起的CHs热脓毒症，这表明人们对OA的病理有了新的认识。
{"title":"Blocking Runx2 Inhibits the Caspase-1 Dependent Pyroptosis in Lipopolysaccharide-Treated Chondrocyte","authors":"Libo Yuan, Ling Yao, Xianzhen Ren, Xusheng Chen, Kaiqiang Kang, Yongqing Xu, Tao Jin","doi":"10.1166/jbn.2024.3765","DOIUrl":"https://doi.org/10.1166/jbn.2024.3765","url":null,"abstract":"Pyroptosis is a new type of cell death in the development of osteoarthritis (OA), but the underlying mechanism is not fully understood. This study aimed to investigate the role of Runx2 in the pyroptosis of chondrocyte (CH) and explore its effect on Caspase-1 expression. Human knee\u0000 tissues from the fracture patients without OA history were collected. Human CHs isolated from the tissue were treated by lipopolysaccharide (LPS) to establish the model of OA. siRNA and CADD522 were used to block the function of Runx2. The cell viability was tested by MTT. The expression levels\u0000 of Runx2, Caspase1/4/5/11, GSDMD, collagen-II, aggrecan, IL-1β, IL-8, and MMP3/9 were detected by RT-PCR, immunofluorescence, or western blot. Besides, the transcriptional association between Runx2 and Caspase-1 was confirmed by DNA immunoprecipitation and luciferase reporter assay.\u0000 Runx2 and Caspase-1 expression were increased in LPS-treated CHs. Runx2 bound to the promoter of Caspase-1 and activated its expression. Moreover, silencing Runx2 or disrupting the DNA-binding ability of Runx2 attenuated the LPS-induced pyroptotic phenotype, containing Caspase-1 activation,\u0000 collagen-II and aggrecan degradation, viability suppression, IL-1β and IL-8 upregulation. Blocking the expression or function of Runx2 alleviated the LPS-caused pyroptosis in CHs in the Caspase-1 manner, indicating a novel understanding of the pathology of OA.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139884140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Relationship between polyethylene targeting nanoparticles and key components of the NOX2/ROS/NF-κB signaling pathway has not yet been fully clarified, and their regulatory role in lung injury in severe acute pancreatitis has not yet been confirmed. In this study, severe acute pancreatitis lung injury cells were exposed to polyethylene targeting nanoparticles and MTT method was used to detect cell proliferation. Cell cycle and apoptosis rate were detected using flow cytometry and the expression of NOX2/ROS/NF-κB pathway was detected. The compound polyethylene targeting nanoparticles inhibited proliferation of lung-damaged cells in severe acute pancreatitis dose-dependently (5, 10 and 20 μmol/L), induced G2/M phase arrest, and increased cell apoptosis. In addition, it reduced the expression of NOX2, ROS, and NF-κB, indicating that NOX2/ROS/NF-κB pathway may be inhibited. Polystyrene targeting nanoparticles reduced the expression of IL-6, TNF-α, JAK, STAT, and IL-10. As a targeted drug delivery system, nano-drug-carrying systems help to dissolve drugs that are difficult to dissolve in the drug solution and intervene in the corresponding tissues and cells in a targeted manner. The results of this study showed that polymer-targeted nano-drug systems could regulate the growth of lung-damaged cells in severe acute pancreatitis. Polyethylene targeting nanoparticles may be effective in inhibiting inflammation in lung-damaged cells in severe acute pancreatitis via regulation of NOX2/ROS/NF-κB pathway.
{"title":"Effect of Polystyrene Targeting Nanoparticles on Lung Injury in Severe Acute Pancreatitis and NOX2/ROS/NF-κB Pathway","authors":"Changbo Liu, Liya Luo, Shuzhen Suo, Yongkang Song","doi":"10.1166/jbn.2024.3783","DOIUrl":"https://doi.org/10.1166/jbn.2024.3783","url":null,"abstract":"Relationship between polyethylene targeting nanoparticles and key components of the NOX2/ROS/NF-κB signaling pathway has not yet been fully clarified, and their regulatory role in lung injury in severe acute pancreatitis has not yet been confirmed. In this study, severe\u0000 acute pancreatitis lung injury cells were exposed to polyethylene targeting nanoparticles and MTT method was used to detect cell proliferation. Cell cycle and apoptosis rate were detected using flow cytometry and the expression of NOX2/ROS/NF-κB pathway was detected. The compound\u0000 polyethylene targeting nanoparticles inhibited proliferation of lung-damaged cells in severe acute pancreatitis dose-dependently (5, 10 and 20 μmol/L), induced G2/M phase arrest, and increased cell apoptosis. In addition, it reduced the expression of NOX2, ROS, and NF-κB,\u0000 indicating that NOX2/ROS/NF-κB pathway may be inhibited. Polystyrene targeting nanoparticles reduced the expression of IL-6, TNF-α, JAK, STAT, and IL-10. As a targeted drug delivery system, nano-drug-carrying systems help to dissolve drugs that are difficult to dissolve\u0000 in the drug solution and intervene in the corresponding tissues and cells in a targeted manner. The results of this study showed that polymer-targeted nano-drug systems could regulate the growth of lung-damaged cells in severe acute pancreatitis. Polyethylene targeting nanoparticles may be\u0000 effective in inhibiting inflammation in lung-damaged cells in severe acute pancreatitis via regulation of NOX2/ROS/NF-κB pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139891310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To enhance the treatment of acute lung injury (ALI) induced by sepsis and optimize the clinical efficacy of simvastatin (SV), we develop SV-loaded nanoliposomes (SV/NLC) as a novel drug delivery system. The NLCs exhibited a particle size of approximately 165 nm, which increased to around 195 nm upon SV loading. NLCs significantly prolonged the half-life of SV by nearly five-fold and improved its penetration into EA.hy926 cells, demonstrating excellent biocompatibility and targeted delivery for ALI therapy. In the rat model of ALI, the SV/NLC effectively reduced the lung wet/dry ratio and the levels of inflammatory factor and albumin in the alveoli, thus improving the alveolar gas exchange function and blood oxygenation. The SV/NLC group demonstrated superior suppression of oxidative stress within lung tissues compared to other groups. Notably, treatment with SV reduction in TLR4, MyD88, and NF-κB P65 levels in lung tissues from ALI rat models. This effect was particularly pronounced in the SV/NLC group. Furthermore, SV can effectively mitigate inflammatory responses and oxidative stress in ALI treatment by modulating the TLR4/NF-κB signaling pathway. In conclusion, our findings suggest that SV can exert therapeutic effects against sepsis-induced ALI through inhibition of the TLR4/NF-κ and mitigate inflammatory response and oxidative stress.
为了加强对脓毒症诱发的急性肺损伤（ALI）的治疗并优化辛伐他汀（SV）的临床疗效，我们开发了一种新型给药系统--SV负载纳米脂质体（SV/NLC）。纳米脂质体的粒径约为 165 nm，载入 SV 后粒径增至约 195 nm。NLCs 将 SV 的半衰期延长了近五倍，并提高了 SV 在 EA.hy926 细胞中的穿透力，证明了其在 ALI 治疗中出色的生物相容性和靶向递送能力。在大鼠 ALI 模型中，SV/NLC 有效降低了肺干湿比以及肺泡中的炎症因子和白蛋白水平，从而改善了肺泡气体交换功能和血氧饱和度。与其他组相比，SV/NLC 组能更好地抑制肺组织内的氧化应激。值得注意的是，SV 治疗降低了 ALI 大鼠肺组织中 TLR4、MyD88 和 NF-κB P65 的水平。这种效应在 SV/NLC 组中尤为明显。此外，SV 还能通过调节 TLR4/NF-κB 信号通路，有效缓解 ALI 治疗过程中的炎症反应和氧化应激。总之，我们的研究结果表明，SV 可通过抑制 TLR4/NF-κ 发挥治疗脓毒症诱发的 ALI 的作用，并减轻炎症反应和氧化应激。
{"title":"A Simvastatin-Loaded Nanoliposome Delivery System for Sepsis-Induced Acute Lung Injury","authors":"Jianhai Yang, Yue Yue","doi":"10.1166/jbn.2024.3805","DOIUrl":"https://doi.org/10.1166/jbn.2024.3805","url":null,"abstract":"To enhance the treatment of acute lung injury (ALI) induced by sepsis and optimize the clinical efficacy of simvastatin (SV), we develop SV-loaded nanoliposomes (SV/NLC) as a novel drug delivery system. The NLCs exhibited a particle size of approximately 165 nm, which increased to around\u0000 195 nm upon SV loading. NLCs significantly prolonged the half-life of SV by nearly five-fold and improved its penetration into EA.hy926 cells, demonstrating excellent biocompatibility and targeted delivery for ALI therapy. In the rat model of ALI, the SV/NLC effectively reduced the lung wet/dry\u0000 ratio and the levels of inflammatory factor and albumin in the alveoli, thus improving the alveolar gas exchange function and blood oxygenation. The SV/NLC group demonstrated superior suppression of oxidative stress within lung tissues compared to other groups. Notably, treatment with SV reduction\u0000 in TLR4, MyD88, and NF-κB P65 levels in lung tissues from ALI rat models. This effect was particularly pronounced in the SV/NLC group. Furthermore, SV can effectively mitigate inflammatory responses and oxidative stress in ALI treatment by modulating the TLR4/NF-κB\u0000 signaling pathway. In conclusion, our findings suggest that SV can exert therapeutic effects against sepsis-induced ALI through inhibition of the TLR4/NF-κ and mitigate inflammatory response and oxidative stress.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139881938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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