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目的:探讨止消通脉宁干预糖尿病肾病小鼠肾间质纤维化作用机制。方法:50只12周龄KKAy小鼠成模后随机分为模型组、厄贝沙坦组、止消通脉宁(ZXTMN)高、中、低剂量组,另设10只C57BL/6为正常组。实验期间,记录小鼠一般状态,血糖,24h尿蛋白定量,血清肌酐(Scr),肾组织Masson染色。Western Blot检测肾α-SMA,TGF-β1,BMP-7和VEGF蛋白表达,实时荧光定量PCR检测肾TGF-β1 mRNA,TGF-βR1 mRNA和Smad2 mRNA表达。结果:与模型组相比较,第4周时,ZXTMN治疗组和厄贝沙坦组小鼠体质量、血糖和24h尿蛋白定量显著性减小(P<0.05),肾间质纤维化评分显著性减低(P<0.05)。ZXTMN高、中组和厄贝沙坦组α-SMA和TGF-β1蛋白表达显著性减少(P<0.01),BMP-7和VEGF蛋白表达显著性增加(P<0.01);ZXTMN各治疗组TGF-β1 mRNA和Smad2 mRNA显著性减少(P<0.01)。结论:调节TGF-β1/Smad抑制肾小管上皮细胞转分化可能是止消通脉宁治疗糖尿病肾病肾间质纤维化的分子机制之一。
Objective: To investigate the mechanism of Zhixiaotongmaining intervening renal interstitial fibrosis in diabetic nephropathy mice. Methods: Fifty KKAy mice of 12 weeks old were randomly divided into model group, irbesartan group and ZXTMN high, medium and low dose groups. Another 10 C57BL / 6 mice were normal group. During the experiment, the general state of mice was recorded, blood glucose, 24h urinary protein, serum creatinine (Scr), Masson staining of renal tissue. The expressions of renal α-SMA, TGF-β1, BMP-7 and VEGF were detected by Western Blot. The expressions of TGF-β1 mRNA, TGF-βR1 mRNA and Smad2 mRNA were detected by real-time fluorescence quantitative PCR. Results: Compared with the model group, the body weight, blood glucose and 24h urinary protein in ZXTMN group and irbesartan group were significantly decreased at the 4th week (P <0.05), and the score of renal interstitial fibrosis was significantly Sex decreased (P <0.05). The expression of α-SMA and TGF-β1 in ZXTMN group was significantly lower than that in ZXTMN group (P <0.01), while the expression of BMP-7 and VEGF protein was significantly increased (P <0.01) β1 mRNA and Smad2 mRNA decreased significantly (P <0.01). CONCLUSION: Regulating the TGF-β1 / Smad inhibition of renal tubular epithelial cell transdifferentiation may be one of the molecular mechanisms in the treatment of renal interstitial fibrosis of diabetic nephropathy.