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作 者:金成山 尤钺 吴艳玲[1] 刘贺 郭建鹏[1] JIN Cheng-shan;YOU Yue;WU Yan-ling;LIU He;GUO Jian-peng(Changbai Mountain Key Laboratory of Biological Resources and Functional Molecules,Ministry of Education,Yanbian University,Yanji 133002,China;Zhejiang Huahai Pharmaceutical Co.,ltd,Linhai 317000,China)
机构地区:[1]延边大学长白山生物资源与功能分子教育部重点实验室,吉林延吉133002 [2]浙江华海药业股份有限公司,浙江临海317000
出 处:《中华中医药杂志》2018年第9期4188-4191,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金项目(No.81660709);吉林省科技发展计划项目(No.20140204034YY)~~
摘 要:目的:考察"千金文武汤"有效组分(QJW)对高糖诱导的人近端肾小管上皮细胞(HK-2)氧化应激的影响。方法:在高糖环境下体外培养HK-2细胞,加入不同比例的有效组分样品,检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力;以Western blot法检测α-平滑肌肌动蛋白(α-SMA)蛋白表达情况。结果:与对照组(NG)比较,高糖组(HG)MDA的含量显著升高(P<0.05);与HG组比较,给药组的MDA含量均下降。HG组SOD活性显著下降(P<0.05),除200μg/mL的6号外,给药组SOD活性升高(P<0.05,P<0.01);NG比较,HG中α-SMA蛋白表达显著升高(P<0.01);与HG比较,给药组细胞α-SMA蛋白含量下降(P<0.01)。结论:QJW能够显著增加细胞SOD活性、减少MDA产生,降低HK-2细胞的α-SMA的表达,从而改善肾纤维化,提高肾功能。Objective: To investigate the effects of Qianjin Wenwu Decoction effective components(QJW) on oxidative stress of human proximal renal tubular epithelial(HK-2) cells induced by high glucose. Methods: HK-2 cells were cultured under high glucose condition in vitro and the contents of malondialdehyde(MDA) and the activity of superoxide dismutase(SOD) were detected after adding different proportion samples of effective components. The expression of α-SMA of HK-2 cells was detected by Western blot. Results: The content of MDA in high glucose(HG) group was obviously increased compared with the normal group(NG)(P〈0.05); the content of MDA in the medication administration group was decreased compared with HG group; the content of SOD in HG group was declined(P〈0.05), and except No.6 of 200μg/mL the content of SOD of other medication administration group were increased(P〈0.05, P〈0.01); the protein content of α-SMA in HG group was increased compared with NG group(P〈0.01); but the medication administration group was decreased compared with HG group(P〈0.01). Conclusion: QJW effective components can enhance the cellular SOD activity, decrease the production of MDA, and downregulate the expression of α-SMA in HK-2 cells.
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