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作 者:宋志霞[1] 饶毅峰[1] 刘阳[1] 夏蓉[1] 徐双双[1] 杨林[1] SONG Zhixia;RAO Yifeng;LIU Yang;XIA Rong;XU Shuangshuang;YANG Lin(Department of Nephrology,the First Clinical College,Three Gorges University/Yichang City Central People′s Hospital,443000 China)
机构地区:[1]宜昌市中心人民医院/三峡大学第一临床医学院肾病内科,湖北宜昌443000
出 处:《西部中医药》2020年第1期13-18,共6页Western Journal of Traditional Chinese Medicine
基 金:国家自然科学基金青年科学基金项目(81600567);宜昌市科学技术局项目(A16-301-02)。
摘 要:目的:探讨黄芪甲苷对糖尿病肾病(diabetic nephropathy,DN)大鼠足细胞裂孔膈膜的保护作用及其可能机制。方法:利用腹腔注射链脲佐菌素(streptozotocin,STZ)建立糖尿病大鼠模型。将40只雄性SD大鼠随机分为4组各10只:正常对照组(NC组)、黄芪甲苷组(astragaloside Ⅳ,AS-Ⅳ组)、糖尿病肾病组(DN组)和糖尿病肾病+黄芪甲苷干预组(DN+AS-Ⅳ组)。造模成功后每6、12周检测大鼠体质量及24小时尿蛋白量。造模后12周末留取大鼠血样本和肾组织标本并处死大鼠。检测大鼠肌酐(serum creatinine,SCr)、尿素氮(blood urea nitrogen,BUN)和尿蛋白;PAS及Masson染色观察肾脏病理改变;电镜观察足细胞超微结构变化;免疫组化法及Western Blot法检测肾组织Nephrin、Podocin、Desmin表达。结果:与DN组相比黄芪甲苷可明显降低大鼠蛋白尿,改善大鼠肾脏病理损伤。DN组Nephrin、Podocin蛋白表达量均低于NC组(P<0.05),Desmin蛋白表达量高于NC组(均P<0.05),AS-Ⅳ组肾脏病理改变及各指标明显改善,差异有统计学意义(P<0.05)。结论:黄芪甲苷可能通过稳定足细胞裂孔隔膜蛋白Nephrin和Podocin来抑制STZ诱导的糖尿病大鼠肾脏损伤。Objective: To explore the protective effects of astragaloside Ⅳ on podocyte impairment of the rats with diabetic nephropathy(DN) and the potential mechanism. Methods: After establishing DM rat models by peritoneal injection of STZ, forty male SD rats were randomized into four groups: normal control group(NC group),astragaloside Ⅳ group(AS-Ⅳ group), DN group and DN+AS-Ⅳ group, ten rats each group. After establishing the rat models successfully, to detect body mass and 24 hours urinary protein content each six and 12 weeks. By the end of 12 weeks, the rats were sacrificed after keeping the samples of blood and renal tissue. To measure SCr, BUN and urinary protein of the rats;PAS and Masson staining were used to observe renal pathological changes;electron microscope was used to observe podocyte ultrastructure changes;immunohistochemical method and Western Blot method were adopted to detect the expressions of Nephrin, Podocin and Desmin in renal tissue. Results: Compared with DN group, astragaloside Ⅳ could obviously reduce proteinuria of the rats, improve renal pathological damage.The expressions of Nephrin and Podocin protein in DN group were lower than these of NC group(P<0.05), Desmin protein expressions were higher than these of NC group(all P <0.05), the chages above in AS-Ⅳ group were notable, and the difference had statistical meaning(P <0.05). Conclusion: Astragaloside Ⅳ could inhibit renal damage of STZ-induced DM rat models by stablizing podocyte slit diaphragm protein Nephrin and Podocin.
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