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作 者:陈铭 莫广艳[2] 叶溪[2] 徐小惠 高雨桐 张晓琳[1] 吴娅妮 韦秀莎 黄仁彬[1] 梁韬 CHEN Ming;MO Guang-yan;YE Xi;XU Xiao-hui;GAO Yu-tong;ZHANG Xiao-lin;WU Ya-ni;WEI Xiu-sha;HUANG Ren-bin;LIANG Tao(Pharmaceutical College,Guangxi Medical University;People′s Hospital of Guangxi Zhuang Autonomous Region;Dept of Pharmacy,Affiliated Tumor Hospital of Guangxi Medical University;Dept of Pharmacy,College&Hospital of Stomatology,Guangxi Medical University;Guangxi Health Commission Key laboratory of Prevention and Treatment for Oral Infectious Diseases,Nanning 530021,China)
机构地区:[1]广西医科大学药学院 [2]广西壮族自治区人民医院 [3]广西医科大学附属肿瘤医院 [4]广西医科大学附属口腔医院 [5]广西壮族自治区卫生健康委员会口腔感染性疾病防治重点实验室,广西南宁530021
出 处:《中国药理学通报》2022年第6期893-897,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 81960671);广西自然科学基金资助项目(No 2018GXNSFBA281037,2018GXNSFBA281096)。
摘 要:目的探讨葛根素(puerarin,PR)对棕榈酸诱导的胰岛MIN6细胞损伤的保护作用及其机制。方法采用不同浓度葛根素预处理细胞2 h,加入120μmol·L^(-1)棕榈酸共同培养24 h建立细胞损伤及凋亡模型。分别采用MTT法、LDH、MDA和GSH试剂盒测定各组细胞的损伤情况,AOEB荧光染色法检测各组细胞凋亡情况;Western blot法检测各组细胞炎症相关蛋白NF-κB、凋亡相关因子Bcl-2、Bax的表达。结果与模型组相比,葛根素各给药组细胞活力、GSH活性升高,LDH、MDA含量降低,p-NF-κB、Bax蛋白表达下调,Bcl-2蛋白表达上调(P<0.05)。结论葛根素可改善棕榈酸诱导的胰岛MIN6细胞的氧化应激状态,进而抑制凋亡和炎症反应而改善胰岛细胞的功能,缓解炎症因子对MIN6细胞的损伤,其可能是通过下调p-NF-κB及Bax蛋白表达,上调Bcl-2蛋白表达实现的。Aim To evaluate the effects of puerarin(PR)on pancreatic islet MIN6 cell injury and apoptosis induced by palmitic acid(PA).Methods MIN6 cells pretreated with 2 h different concentrations of PR were then co-cultured with 120μmol·L^(-1) PA for 24 h to establish the cell injury and apoptosis model.MTT,LDH,MDA and GSH were used to determine the damage of MIN6 cells.AOEB fluorescence staining was used to detect the apoptosis of MIN6 cells.Western blot was used to detect the expressions of inflammation-related protein NF-κB,apoptosis-related factors Bcl-2 and Bax.Results Compared with model group,cell viability and GSH activity of puerarin administration groups increased,LDH and MDA contents decreased,the protein expressions of p-NF-κB and Bax were down-regulated,and the protein expressions of Bcl-2 were up-regulated(P<0.05).Conclusions Puerarin can improve the function of pancreatic islet cells by inhibiting apoptosis and inflammation,and ameliorate pancreatic islet MIN6 cell injury and apoptosis induced by palmitic acid-induced,alleviate MIN6 cell injury induced by inflammatory factors,which may be achieved by down-regulating the expression of p-NF-κB and Bax proteins,and up-regulating the expression of Bcl-2 protein.
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