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目的观察益气养阴消癥通络中药对糖尿病肾病(DN)大鼠TGF-β/Smads信号传导系统的影响。方法选择46只健康雄性SD大鼠,随机分为对照组10只,造模组36只。除对照组外,造模组大鼠1次性ip链脲佐菌素(STZ)60 mg/kg,造模组在糖尿病模型成模后,随机分为模型组、贝那普利组、中药组。成模1周后开始给药,贝那普利组以10 mg/(kg.d)ig给药,中药组以26 g/(kg.d)ig给药,各组连续给药23周后处死动物。HE、PAS染色观察组织病变程度,免疫组化检测TGF-β1、p-Smad2/3的改变,Western-blotting检测Smad7蛋白表达水平。结果与模型组相比,益气养阴消癥通络中药能够显著减轻DN大鼠肾组织病理损害,免疫组化以及Westernblotting显示,益气养阴消9通络中药能够显著下调TGF-β1、p-Smad2/3蛋白的表达,上调Smad7蛋白的表达。结论益气养阴消癥通络中药能够减轻DN的病理损害,这一作用的实现可能是部分通过TGF-β/Smads信号传导途径实现的,即降低受体激活型Smad表达,上调抑制型Smad7表达。
Objective To observe the effect of Yiqi Yangyin Xiaozheng Tongluo Chinese medicine on TGF-β/Smads signal transduction system in diabetic nephropathy (DN) rats. Methods Forty-six healthy male Sprague-Dawley rats were randomly divided into control group and model group. In addition to the control group, rats in the modeling group were given a single dose of IP streptozotocin (STZ) 60 mg/kg. The model group was randomly divided into a model group, a benazepril group, and a Chinese medicine after the diabetes model was completed. group. One week after the completion of the injection, the benazepril group was administered with 10 mg/(kg.d)ig, and the Chinese medicine group was administered with 26 g/(kg.d)ig. Each group was given continuous administration for 23 weeks. Animals were sacrificed. HE and PAS staining were used to observe the degree of tissue lesions. The changes of TGF-β1 and p-Smad2/3 were detected by immunohistochemistry. The expression of Smad7 protein was detected by Western-blotting. Results Compared with the model group, the traditional Chinese medicine of supplementing Qi and nourishing yin clearing away can significantly reduce the pathological damage of kidney tissue in DN rats. Immunohistochemistry and Western blotting showed that Yiqi Yangyinxiao 9 Tongluo can significantly down-regulate TGF-β1. The expression of p-Smad2/3 protein up-regulated the expression of Smad7 protein. Conclusion Yiqi Yangyin Xiaozheng Tongluo medicine can reduce the pathological damage of DN. This effect may be achieved partly through the TGF-β/Smads signal transduction pathway, that is, reduce the expression of receptor-activated Smad and up-regulate the inhibitory Smad7. expression.