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目的分析补体C3a(complement 3a)及其受体C3aR(complement 3a receptor)在马兜铃酸Ⅰ(Aristolochic acid I,AAI)肾损伤大鼠体内的表达情况,初步探究其在马兜铃酸肾病中的作用。方法 SD大鼠按体质量完全随机分为溶媒对照组,AAI低、高剂量(2.25,9.00 mg·kg~(-1))组,连续腹腔注射给药14 d,取血清,检测肌酐(serum creatinine,Scr)、尿素氮(blood urea nitrogen,BUN)、补体C3、C3a;用HE法染色观察肾脏病理组织学变化;用蛋白免疫印迹(Western Blot)法分析肾脏组织C3aR蛋白的表达;用免疫组织化学方法分析肾脏组织C3aR的表达变化。结果与溶媒对照组比较,AAI低、高剂量组Cr、BUN水平显著升高(P<0.05,P<0.01);补体C3水平显著降低(P<0.01),而C3a水平显著升高(P<0.05,P<0.01);肾脏病理学检查显示AAI低、高剂量组肾脏有明显病变;Western Blot结果显示,与溶媒对照组比较,AAI低、高剂量组大鼠肾脏中C3aR蛋白表达水平明显升高,且呈剂量依赖关系,差异有统计学意义(P<0.01);免疫组化分析显示,溶媒对照组肾组织中可在肾小管上皮细胞见C3aR少量表达,AAI低、高剂量组的大鼠肾组织中C3aR主要表达在肾小管上皮细胞和间质细胞等,且C3aR表达显著高于溶媒对照组(P<0.01),随病理损伤程度增加而增多。结论C3aR在AAI致肾损伤大鼠肾脏组织中有表达,通过与其配体结合可能引起肾组织的损伤。补体C3a及其受体在马兜铃酸肾病中发挥一定的作用。
Objective To investigate the expression of complement 3a and complement 3a receptor in rat models of aristolochic acid I (AAI) injury and to investigate the role of complement 3a and its complement C3a in aristolochic acid nephropathy Role. Methods SD rats were randomly divided into vehicle control group, AAI low dose and high dose (2.25, 9.00 mg · kg -1) groups. The rats were given intraperitoneal injection for 14 days. Serum was taken and serum creatinine creatinine, Scr, BUN, C3, C3a. The renal histopathological changes were observed by HE staining. The expression of C3aR protein in kidney tissues was analyzed by Western Blot. Changes of C3aR Expression in Renal Tissues by Histochemistry. Results Compared with the vehicle control group, the levels of Cr and BUN in low and high AAI groups were significantly increased (P <0.05, P <0.01), while the level of complement C3 was significantly lower (P <0.01) and C3a levels were significantly higher (P < 0.05, P <0.01). Kidney pathological examination showed that the kidneys in low and high AAI group had obvious lesions. Western Blot showed that the expression of C3aR protein in kidney of AAI low and high dose groups was significantly higher than that of vehicle control group (P <0.01). Immunohistochemical analysis showed that small amount of C3aR was expressed in renal tubular epithelial cells in the vehicle control group, and the expression of C3aR in renal tubular epithelial cells was lower in the AAI group than in the control group The expression of C3aR in rat kidney was mainly expressed in renal tubular epithelial cells and stromal cells, and the expression of C3aR was significantly higher than that in vehicle control group (P <0.01), which increased with the degree of pathological injury. Conclusion C3aR is expressed in the kidney tissue of AAI-injured rats, which may result in the damage of renal tissue by binding with its ligand. Complement C3a and its receptors play a role in aristolochic nephropathy.