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作 者:胡梅芬[1] 苏双全[1] 赵莉[1] 夏林[1] 吴永贵[1]
机构地区:[1]安徽医科大学第一附属医院肾脏内科,合肥230022
出 处:《临床肾脏病杂志》2012年第4期178-181,共4页Journal Of Clinical Nephrology
基 金:教育部高等学校博士学科点专项科研基金(20093420110003)
摘 要:目的探讨白芍总苷(TGP)对糖尿病大鼠肾小管-间质细胞转分化的影响。方法建立链脲佐菌素(STZ)诱导的大鼠糖尿病模型,将大鼠随机分对照组、模型组、TGP给药组(50、100、200mg·kg-1·d-1灌胃),8w后观察肾小管-间质损伤指数(TII)的变化,应用免疫组化方法检测肾组织E-钙黏蛋白(E-cadherin,E-cad)、α平滑肌肌动蛋白(a-smooth muscleactin,α-SMA)以及波形蛋白(Vim—entin,Vh)的表达。结果TGP给药呈剂量依赖性降低糖尿病大鼠24h尿白蛋白排泄率。模型组TⅡ明显高于对照组,TGP给药组(100mg·kg-1·d-1与200mg·kg-1·d-1)TII明显低于模型组。模型组肾小管-间质E-cad表达明显低于对照组(P〈0.05),TGP50、100、200mg·kg-1·d-1给药组E-cad表达明显高于模型组(P〈0.01)。模型组肾小管-间质α—SMA与Vim蛋白表达明显高于对照组(P〈0.叭),TGP50、100、200mg·kg-1·d-1给药组肾小管-间质α-SMA与Vim蛋白表达明显低于模型组(P〈0.01)。结论TGP可降低肾小管-间质α—SMA和vim的表达,增加E—cad的表达,抑制肾小管-间质细胞转分化。Objective To investigate the effect of total glucosides of paeony (TGP) on transdifferen- tiation of renal tubulointerstitial cells in diabetic rats. Methods Diabetes was induced by injection of strepto- zotocin in rats. Rats were randomly divided into three groups: control group, model group, TGP group. TGP (50, 100,200 mg·kg-1·d-1 ) was orally administered once a day for 8 weeks. Tubulointerstitial mor- phological changes were observed in PAS-stained sections. The expression of E-cadherin (E-cad), a-smooth muscle actin (α-SMA) and vimentin (Vim) in renal tubulointerstitium was detected by using immunohisto- chemistry. Results Elevated 24-h urinary albumin excretion rate was markedly attenuated by TGP treatment with 50, 100 and 200 mg.·kg-1·d-1 in diabetic rats. Increased indices for tubulointerstitial injury were sig- nificantly ameliorated by TGP treatment with 100 and 200 mg·kg-1·d-1 in diabetic rats (P〈0.05, 0. 01 ). In renal tubulointerstitium in diabetic rats, decreased expression of E-cad protein was significantly inhibited by TGP treatment with 50, 100 and 200 mg·kg-1·d-1(P〈0. 01) and elevated expression ofα-SMA and Vim protein was also significantly inhibited by TGP treatment with 50, 100 and 200mg·kg-1·d-1(P〈 0. 01 ). Conclusions TGP can down-regulate the expression of a-SMA and Vim, and up-regulate the expres- sion of E-cad in diabetic renal tubulointerstitial cells and restrain the process of tubulointerstitial cells trans- differentiation in diabetic rats.
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