【摘 要】
：
目的 观察水陆地黄胶囊对糖尿病肾病(diabetic kidney disease,DKD)大鼠的治疗作用,并验证该药物是否可通过激活LKB1-AMPK-Sirt1信号通路增强足细胞自噬活性并改善DKD.方法 60只SD大鼠腹腔注射链脲佐菌素制成DKD大鼠模型,随机分为模型组、西药组、中药组,正常组与模型组大鼠每日予以生理盐水灌胃,西药组予以贝那普利药液灌胃,中药组予以水陆地黄胶囊药液灌胃.干预后检测血糖、血肌酐、尿素氮、24小时尿微量白蛋白等DKD相关指标;肾脏HE染色、Masson染色观察病理变化;透
【机 构】
：
712046 咸阳,陕西中医药大学第一临床医学院
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目的 观察水陆地黄胶囊对糖尿病肾病(diabetic kidney disease,DKD)大鼠的治疗作用,并验证该药物是否可通过激活LKB1-AMPK-Sirt1信号通路增强足细胞自噬活性并改善DKD.方法 60只SD大鼠腹腔注射链脲佐菌素制成DKD大鼠模型,随机分为模型组、西药组、中药组,正常组与模型组大鼠每日予以生理盐水灌胃,西药组予以贝那普利药液灌胃,中药组予以水陆地黄胶囊药液灌胃.干预后检测血糖、血肌酐、尿素氮、24小时尿微量白蛋白等DKD相关指标;肾脏HE染色、Masson染色观察病理变化;透射电镜观察自噬泡的形成;Western blot检测肾脏组织Bcl-2相互作用蛋白(Bcl-2 interacting coiled-coil protein 1,Beclin-1)、微管相关蛋白1轻链3(microtubule associated protein 1 light chain 3,LC3II/I)、肝激酶B1(liver kinase B1,LKB1)、腺苷酸激活蛋白激酶[AMP-activated protein kinase,AMPK/p-AMPK]、沉默信息调节因子-1(silent information regulator-1,Sirt 1)蛋白的表达.结果 与正常组相比,造模2周后造型组中46只大鼠空腹血糖≥6.7 mmol/L,提示造模成功;给药8周后模型组、西药组、中药组的血糖进一步升高(P0.05).与正常组相比,模型组、西药组、中药组24小时尿蛋白明显升高(P>0.05);与模型组相比,西药组、中药组的24小时尿蛋白明显下降(P0.05).HE染色:与模型组比较,西药组、中药组肾脏组织病变较模型组减轻,有少量炎性细胞浸润系膜增生;Masson染色:与模型组比较,西药组、中药组肾脏组织病变减轻.电镜下观察:正常组细胞内结构正常,可见明见自噬泡;模型组细胞结构破坏,自噬泡较少;中药组、中西药组自噬泡增多,提示自噬增强.Western blot检测:与模型组相比,中药组、西药组肾脏组织中Beclin-1、LC3Ⅱ/Ⅰ、LKB1、p-AMPK、Sirt1表达均明显升高(P0.05).结论 水陆地黄胶囊能降低糖尿病肾病大鼠血糖,改善肌酐、尿素氮,减少蛋白尿,其机制可能是激活LKB1/AMPK/Sirt1信号通路增强足细胞自噬活性.
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