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目的:观察抗α1肾上腺素能受体自身抗体(α1-AA)对大鼠24h微量白蛋白(24hUpro)、血清肌酐(Scr)、肾脏结构及IV型胶原、Smad2/3蛋白等的影响。方法:采用α1-AA注射液100μg/100g于实验第0、4、8、12、16周经鼠尾静脉注射DM大鼠(免疫介导组),并设不行α1-AA注射的DM大鼠为对照组(无介导组)。ELISA检测两组抗α1-AA阳性率;常规方法检测两组24hUpro和Scr;电镜观察两组大鼠肾脏病理变化,免疫组化法检测两组大鼠肾组织中IV型胶原、Smad2/3蛋白分布及表达;并用受体阻断剂干预受体阳性大鼠(干预组)后,观察以上指标的变化。结果:(1)免疫介导组α1-AA阳性率91.67%(22/24),明显高于无介导组(27.30%),差异有统计学意义(P<0.01)。(2)免疫介导组大鼠Scr和24hUpro明显高于无介导组,差异亦有统计学意义(P<0.01),干预组大鼠Scr和24hUpro较免疫介导组明显改善(P<0.01)。(3)电镜下α1-AA介导组大鼠肾组织损伤严重,无介导组损伤不明显,干预组较免疫介导组病变明显减轻。(4)免疫介导组肾组织IV型胶原、Smad2/3蛋白表达显著高于无介导组(P<0.05),干预组上述表达明显减少,与免疫介导组差异具有统计学意义(P<0.01)。结论:通过免疫介导可以建立具激动样活性的抗α1肾上腺素受体抗体的大鼠模型;抗α1-AA介导可致糖尿病大鼠肾基质重构,参与糖尿病肾脏损害的病理生理过程;受体拮抗剂可改善和逆转肾损害。
OBJECTIVE: To observe the effects of anti-α1 adrenergic receptor autoantibodies (α1-AA) on 24 h microalbuminuria (24hUpro), serum creatinine (Scr), renal structure, type IV collagen and Smad2 / 3 protein in rats. Methods: DM rats (immune-mediated group) were injected via the tail vein of mice with 100μg / 100g α1-AA injection at 0, 4, 8, 12 and 16 weeks, For the control group (no mediated group). ELISA was used to detect the positive rate of α1-AA in both groups. The 24hUpro and Scr were detected by routine methods. The renal pathological changes of the two groups were observed by electron microscope. The expressions of type IV collagen and Smad2 / 3 protein in kidney were detected by immunohistochemistry Distribution and expression; and receptor blocker intervention receptor positive rats (intervention group), observe the above indicators changes. Results: (1) The positive rate of α1-AA in immune-mediated group was 91.67% (22/24), significantly higher than that in non-mediated group (27.30%), the difference was statistically significant (P <0.01). (2) Scr and 24hUpro in the immune-mediated group were significantly higher than those in the non-mediated group (P <0.01), and Scr and 24hUpro in the intervention group were significantly improved compared with the immunocompetent group (P <0.01) ). (3) The damage of renal tissue in α1-AA-mediated rats was serious under electron microscope. The damage of non-mediated group was not obvious. Compared with the immune-mediated group, the lesions in the intervention group were significantly reduced. (4) The expression of type IV collagen and Smad2 / 3 in renal tissue of immune-mediated group was significantly higher than that in non-mediated group (P <0.05), and the expression of Smad2 / 3 in immune-mediated group was significantly decreased <0.01). CONCLUSION: A rat model of anti-α1-adrenergic receptor with agonistic activity can be established by immune mediation. Anti-α1-AA mediated renal matrix remodeling in diabetic rats may be involved in the pathophysiological process of diabetic nephropathy. Receptor antagonists can improve and reverse renal damage.