首页> 中文期刊> 《安徽医科大学学报》 >白芍总苷对糖尿病大鼠肾组织Txnip、Trx与ASK1表达的调节作用

白芍总苷对糖尿病大鼠肾组织Txnip、Trx与ASK1表达的调节作用

         

摘要

目的:了解白芍总苷( TGP)对糖尿病大鼠肾组织硫氧还蛋白相互作用蛋白( Txnip)、硫氧还蛋白( Trx)与凋亡信号激酶1(ASK1)表达的影响,探讨TGP对糖尿病肾组织Trx系统调节作用。方法将链脲佐菌素( STZ)诱导的糖尿病大鼠随机分为模型组、TGP [50、100、200 mg/(kg·d)]给药组,另取正常大鼠为对照组,8周后测定大鼠尿白蛋白排泄率( UAER)。应用免疫组化、Western blot法及实时定量PCR法检测大鼠肾组织Txnip、Trx与ASK1表达。结果实验8周后TGP[50、100、200 mg/(kg·d)]给药组及对照组大鼠UAER水平均低于模型组(P<0.01);免疫组化和(或)West-ern blot法显示TGP [50、100、200 mg/(kg·d)]给药组及对照组大鼠肾组织Txnip、ASK1表达低于模型组( P<0.05,P<0.01),而Trx高于模型组(P<0.05,P<0.01);实时定量PCR显示TGP [50、100、200 mg/(kg·d)]给药组及对照组Txnip mRNA低于模型组(P<0.01,P<0.05),Trx mRNA高于模型组(P<0.01,P<0.05)。结论糖尿病肾病大鼠肾组织存在Trx系统异常,TGP对糖尿病大鼠肾组织保护作用可能与抑制Txnip表达、提高Trx表达有关。%Objective To research effect of total glucosides of paeony ( TGP) on the expression of thioredoxin-in-teracting protein (Txnip), thioredoxin(Trx)and apoptosis signal-regulating kinase 1 (ASK1) investigate role of TGP on thioredoxin system in the kidney from diabetic rats. Methods Diabetes rats induced with streptozotocin were randomly divided into model group which was treated with TGP [50,100,200 mg/(kg·d),for 8 weeks];besides,use normal rats as control group. 24 h urinary albumin excretion rate( UAER) was determined with ELISA. Txnip,Trx and ASK1 were measured with immunohischemistry, Western blot and real-time PCR. Results Elevat-ed 24 h UAER was obviously decreased by TGP treatment with 50, 100,200 mg/(kg·d). Compared with diabetic rats, analysis of the immunohischemistry and/or Western blot showed the expression of Txnip and ASK1 was de-creased in TGP treatment with 50, 100, 200 mg/(kg·d) (P<0. 01), and the expression of Trx was increased(P<0. 01 ) . Real-time PCR analysis showed that Txnip mRNA expression in diabetic rats was also significantly inhib-ited by TGP (P<0. 05), and that Trx mRNA was markedly increased by TGP(P<0. 05). Conclusion There is an abnormity occuring in the thioredoxin system in the renal tissue of diabetic rats. TGP obviously has the function of renal protection,and its mechanism may be related to the inhibition of Txnip expression and the enhancement of Trx expression.

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