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作 者:马石楠[1] 郭海珍 刘婷 朱景鸣 蒋宏宽 王小莉[1] MA Shi-nan;GUO Hai-zhen;LIU Ting;ZHU Jing-ming;JIANG Hong-kuan;WANG Xiao-li(Key Laboratory of Embryonic Stem Cell Research of Hubei Province,Taihe Hospital,Hubei University of Medicine,Shiyan,Hubei 442000,China)
机构地区:[1]湖北医药学院附属太和医院胚胎干细胞研究湖北省重点实验室,湖北十堰442000
出 处:《湖北医药学院学报》2023年第2期137-142,F0003,共7页Journal of Hubei University of Medicine
基 金:湖北省科技厅面上项目(2022CFB446);湖北省教育厅重点项目(D20222108);大学生创新创业训练项目(S202110929025)。
摘 要:目的:探讨间充质干细胞外泌体(MSC-Exos)联合肝再生增强因子(ALR15)mRNA对对乙酰氨基酚(APAP)诱导的肝细胞凋亡的影响。方法:通过NAT粒径检测、TEM电镜检测以及Western Blot鉴定提取的MSCExos。通过免疫荧光和Western Blot鉴定体外合成ALR15 mRNA。通过荧光染色、流式细胞术和Western Blot检测外泌体联合ALR15 mRNA对APAP引起的肝细胞凋亡的影响。结果:成功分离获得了MSC-Exos,并体外成功合成了ALR15 mRNA。外泌体联合ALR15 mRNA可进入肝细胞,通过抑制ROS的生成使APAP诱导的肝细胞凋亡减轻,且外泌体联合ALR15 mRNA比仅添加外泌体的抗凋亡效果更好。结论:MSC-Exos联合ALR mRNA可通过抑制ROS产生减轻APAP诱导的肝细胞凋亡,为干细胞外泌体联合ALR15 mRNA治疗APAP引起的肝细胞凋亡提供一个新的治疗思路。Objective To investigate the effect of mesenchymal stem cell exosomes(MSC-Exos)combined with Augmenter of liver regeneration(ALR15)mRNA on Acetaminophen(APAP)-induced hepatocyte apoptosis.Methods MSC-Exos were characterized by NAT particle size detection,transmission electron microscopy(TEM)and Western Blot.The in vitro synthesized ALR15 mRNA was identified by immunofluorescence and Western Blot.The effects of MSC-Exos combined with ALR15 mRNA on APAP-induced hepatocytes apoptosis were detected by fluorescence staining,flow cytometry and Western Blot.Result MSC-Exos were successfully isolated and ALR15 mRNA was successfully synthesized in vitro.MSCExos combined with ALR15 mRNA could entere the APAP treated hepatocytes and significantly reduced the cell apoptosis through inhibiting the ROS production.The anti-apoptosis effect of exosomes combined with ALR15 mRNA was better than that of only exosomes.Conclusion The MSC-Exos combined with ALR mRNA can alleviate APAP-induced hepatocyte ap⁃optosis by inhibiting ROS production,which provides a new therapeutic idea for the treatment of APAP-induced hepatocyte apoptosis with stem cell exosomes combined with ALR15 mRNA.
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