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目的观察依那西普靶点治疗对T2DM大鼠肾组织肿瘤坏死因子相关的凋亡诱导配体(TRAIL)系统表达的影响,探讨其肾脏保护作用机制。方法建立T2DM大鼠模型。成模后将大鼠随机分为4组:正常对照(NC)组、模型对照(T2DM)组、阿托伐他汀治疗(DA)组、依那西普治疗(DE)组。用ELISA、免疫组化、Q-RT-PCR法等分别检测尿α1-微球蛋白(Uα1-MG)、血清TNF-α,及TNF-α、TRAIL、死亡受体4(DR4)、诱骗受体2(DcR2)在肾组织表达。结果与NC组比,各时间点DM组大鼠Uα1-MG、血清TNF-α显著升高(P<0.01),肾组织TNF-α、DcR2表达显著增强(P<0.01);而TRAIL、DR4表达(P<0.01)显著减弱。治疗后各指标均呈相反改变。与DA组比较,DE组大鼠Uα1-MG、血清TNF-α降低更显著(P<0.01)。与DE组比较,治疗后DA组大鼠肾组织TNF-α、TRAIL、DR4表达增强(P<0.01,P<0.05),DcR2表达减弱(P<0.01)。结论靶点治疗通过影响TNF-α及TRAIL系统的表达,对T2DM大鼠具有显著的肾脏保护作用。
Objective To observe the effect of etanercept target therapy on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) system expression in renal tissues of T2DM rats and to explore its mechanism of renal protective effect. Methods T2DM rat model was established. After modeling, the rats were randomly divided into 4 groups: normal control (NC) group, model control (T2DM) group, atorvastatin treatment (DA) group and etanercept treatment group (DE). Urine α1-microglobulin (Uα1-MG), serum TNF-α, TNF-α, TRAIL and DR4 were detected by ELISA, immunohistochemistry and Q-RT- Body 2 (DcR2) is expressed in kidney tissue. Results Compared with NC group, Uα1-MG and TNF-α in DM group were significantly increased (P <0.01) and TNF-α and DcR2 expression in renal tissue were significantly increased at each time point (P <0.01) Expression (P <0.01) was significantly weakened. After treatment, the indicators were the opposite change. Compared with DA group, the decrease of Uα1-MG and serum TNF-α in DE group was more significant (P <0.01). Compared with DE group, the expression of TNF-α, TRAIL and DR4 increased (P <0.01, P <0.05) and the expression of DcR2 decreased (P <0.01). Conclusion Targeting therapy has significant renal protective effect on T2DM rats by affecting the expression of TNF-α and TRAIL.