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目的探讨西格列汀(SIT)延缓或阻止2型糖尿病肾病(DN)进展的作用及其可能机制。方法高脂饲养加小剂量链脲佐菌素诱导建立大鼠DN模型,成模后,随机分为模型组(DN组)和西格列汀组(SIT组),同时设立对照组(NC组)。连续灌胃12周后,取肾组织进行Masson染色检测肾纤维化程度,用反转录PCR法检测肾组织中Toll样受体2(TLR2)、TLR4、核转录因子-κB(NF-κB)mRNA的表达,用免疫组化法检测肾组织中TLR2、TLR4蛋白的含量,用Western blotting法检测肾组织中NF-κB蛋白的含量。结果与NC组相比,DN组的肾纤维化程度、TLR2、TLR4、NF-κB的表达均显著增加(P<0.01)。与DN组相比,SIT组的肾纤维化程度、TLR2、TLR4、NF-κB的表达均有所降低(P<0.05)。结论西格列汀可改善2型糖尿病大鼠的肾纤维,其机制可能与抑制TLR2、TLR4/NF-κB通路的过度活化有关。
Objective To investigate the role of sitagliptin (SIT) in retarding or preventing the progression of type 2 diabetic nephropathy (DN) and its possible mechanism. Methods The model of DN was established by high fat diet and small dose of streptozotocin (STZ). The rats were randomly divided into model group (DN group) and sitagliptin group (SIT group), and the control group (NC group) ). After 12 weeks of continuous gavage, the renal tissue was taken for Masson staining to detect the degree of renal fibrosis. Toll-like receptor 2 (TLR2), TLR4, nuclear factor-kappa B (NF-κB) The mRNA expression of TLR2 and TLR4 in renal tissues was detected by immunohistochemistry. The content of NF-κB in renal tissues was detected by Western blotting. Results Compared with NC group, the degree of renal fibrosis, the expressions of TLR2, TLR4 and NF-κB in DN group were significantly increased (P <0.01). Compared with DN group, the degree of renal fibrosis, TLR2, TLR4 and NF-κB expression in SIT group were decreased (P <0.05). Conclusion Sitagliptin can improve renal fibrosis in type 2 diabetic rats. The mechanism may be related to the inhibition of TLR2, TLR4 / NF-κB pathway over-activation.