论文部分内容阅读
目的:观察ApoAI/ABCA1途径对糖尿病肾病炎症反应是否有调节作用。方法:选用SD大鼠40只随机分为4组,每组10只,分别为:正常对照组、糖尿病肾病(DN)组、DN+载脂蛋白-I(ApoA-I)组、DN+绿色荧光蛋白(GFP)组。除正常对照组外,其它3组腹腔注射链脲佐菌素(STZ,65 mg/kg)溶液造糖尿病大鼠模型。DN+ApoA-I组在糖尿病造模成功后尾静脉注射腺病毒AdV-AI;DN+GFP组在糖尿病造模成功后通过尾静脉注射腺病毒Ad V-GFP,方法同DN+ApoA-I组。观察各组大鼠血清肿瘤坏死因子-α(TNF-α)、MCP-1,肾组织抗炎蛋白(锌指蛋白36,TTP)表达及ABCA1 mRNA表达。结果:相对于对照组,DN组、DN+ApoA-I组、DN+GFP组大鼠血清中的TNF-α、MCP-1水平明显上升(P<0.05);相对于DN组,DN+ApoA-I组的TNF-α、MCP-1水平明显下降(P<0.05);相对于对照组,DN组TTP蛋白、ABCA1 mRNA的表达量有所降低(P<0.05);相对于DN组,DN+ApoA-I组大鼠肾组织TTP蛋白、ABCA1 mRNA的表达明显升高(P<0.05);DN+GFP组大鼠TTP蛋白、ABCA1 mRNA的表达与DN组相比无明显变化。结论:ApoA-I/ABCA1途径是体内抗DN炎症激活的关键作用途径,其机制可能通过上调TTP,从而促进多种炎症因子的降解。
Objective: To investigate whether ApoAI / ABCA1 pathway can regulate the inflammatory reaction of diabetic nephropathy. Methods: Forty SD rats were randomly divided into 4 groups (n = 10): normal control group, diabetic nephropathy group, DN + apolipoprotein-I group, DN + green fluorescent protein (GFP) group. In addition to the normal control group, the other three groups were intraperitoneally injected with streptozotocin (STZ, 65 mg / kg) solution to make diabetic rat model. DN + ApoA-I group was injected with adenovirus AdV-AI after tail vein injection in diabetic model. DN + GFP group was injected with adenovirus Ad V-GFP through tail vein after successful diabetes mellitus. . The levels of tumor necrosis factor-α (TNF-α), MCP-1, renal tissue anti-inflammatory protein (zinc finger protein 36, TTP) and ABCA1 mRNA expression in each group were observed. Results: The levels of TNF-α and MCP-1 in DN group, DN + ApoA-I group and DN + GFP group were significantly higher than those in control group (P <0.05) (P <0.05). Compared with the control group, the expressions of TTP and ABCA1 mRNA in DN group were decreased (P <0.05). Compared with DN group, the levels of TNF-α and MCP- + TTP protein and ABCA1 mRNA expression in renal tissue of ApoA-I group were significantly increased (P <0.05). The expression of TTP protein and ABCA1 mRNA in DN + GFP group had no significant change compared with DN group. CONCLUSION: The ApoA-I / ABCA1 pathway is a key pathway in anti-DN inflammation in vivo. The mechanism may be through the up-regulation of TTP, which may promote the degradation of multiple inflammatory cytokines.