膜肾方调控C3a/C3aR通路对特发性膜性肾病大鼠血浆诱导损伤足细胞的影响*

作者：丁 秀1,2,3,4，李 慧1,2,3,4，刘会彬1,2,3,4，吴成态1,2,3,4，王小琴1,2,3,4，邹新蓉1,2,3,4

单位：1.湖北省中医院，湖北 武汉 430061； 2.湖北中医药大学附属医院，湖北 武汉 430061； 3.湖北省中医药研究院，湖北 武汉 430061； 4.中医肝肾研究及应用湖北省重点实验室，湖北 武汉 430061

引用：引用：丁秀，李慧，刘会彬，吴成态，王小琴，邹新蓉.膜肾方调控C3a/C3aR通路对特发性膜性肾病大鼠血浆诱导损伤足细胞的影响[J].中医药导报,2026,32(3):1-5.

DOI：10.13862/j.cn43-1446/r.2026.03.001

PDF： 下载PDF

摘要：

目的：探讨膜肾方对特发性膜性肾病大鼠血浆诱导损伤足细胞的干预作用及其机制。方法：建立特发性膜性肾病大鼠模型，用肝素钠作为抗凝剂收集其血浆样品并诱导足细胞损伤，分对照组、模型组、膜肾方组、膜肾方+C3a受体（C3aR）拮抗剂组、C3aR拮抗剂组。采用Western blotting检测各组足细胞C3aR、磷脂酶A2受体（PLA2R）、磷酸化细胞外信号调节激酶1/2（p-ERK1/2）、磷酸化细胞浆型磷脂酶A2（p-cPLA2）蛋白表达水平；酶联免疫吸附试验（ELISA）检测上清液C3a表达水平；Real-time PCR测定Synaptopodin mRNA、C3aR mRNA、PLA2R mRNA表达水平；细胞计数试剂盒-8（CCK-8）检测各组足细胞活力。结果：与对照组比较，模型组足细胞C3aR、PLA2R、p-ERK1/2、p-cPLA2表达水平均升高，上清液C3a水平升高，Synaptopodin mRNA水平下降，C3aR mRNA、PLA2R mRNA水平升高，足细胞活力下降，差异均有统计学意义（P＜0.01）；与模型组比较，膜肾方组足细胞C3aR、PLA2R、p-ERK1/2、p-cPLA2表达水平均下降，上清液C3a水平下降，Synaptopodin mRNA水平升高，C3aR mRNA、PLA2R mRNA水平下降，足细胞活力改善，差异均有统计学意义（P＜0.01）；与膜肾方组比较，膜肾方+C3aR拮抗剂组及C3aR拮抗剂组足细胞C3aR、PLA2R、p-ERK1/2、p-cPLA2表达水平均下降，上清液C3a水平下降，Synaptopodin mRNA水平升高，C3aR mRNA、PLA2R mRNA水平下降，足细胞活力改善，膜肾方+C3aR拮抗剂组更明显，差异均有统计学意义（P＜0.01）。结论：膜肾方可能通过调控C3a/C3aR通路，下调PLA2R水平，稳定足细胞骨架，改善足细胞活力，从而发挥对足细胞的保护作用。

关键词：特发性膜性肾病；膜肾方；足细胞；C3a/C3aR通路

Abstract：

Objective: To investigate the protective effect of Moshen Formula on podocytes injured by plasma from rats with idiopathic membranous nephropathy (IMN) and to explore its underlying mechanism. Methods: An IMN rat model was established. Plasma samples, collected using heparin sodium as an anticoagulant, were used to induce podocyte injury in vitro. The experimental groups included a control group, a model group, a Moshen Formula group, a Moshen Formula+C3aR antagonist group, and a C3aR antagonist group. Western blotting was used to detect the protein expression levels of C3aR, phospholipase A2 receptor (PLA2R), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated cytosolic phospholipase A2 (p-cPLA2). The concentration of C3a in the supernatant was measured by enzyme-linked immunosorbent assay (ELISA). The expression levels of Synaptopodin mRNA, C3aR mRNA, and PLA2R mRNA were quantified using real-time PCR. Podocyte viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Results: Compared with the control group, the model group exhibited significant increases in the protein expression of C3aR, PLA2R, p-ERK1/2, and p-cPLA2; higher supernatant C3a levels; reduced Synaptopodin mRNA expression; upregulated C3aR mRNA and PLA2R mRNA expression; and decreased podocyte viability (P<0.01). Compared with the model group, the Moshen Formula group showed significant downregulation of C3aR, PLA2R, p-ERK1/2, and p-cPLA2 protein levels; decreased supernatant C3a; increased Synaptopodin mRNA; reduced C3aR mRNA and PLA2R mRNA; and improved podocyte viability (P<0.01). Compared with the Moshen Formula group, both the Moshen Formula+C3aR antagonist group and the C3aR antagonist group showed downregulation of C3aR, PLA2R, p-ERK1/2, and p-cPLA2 protein levels; decreased supernatant C3a; increased Synaptopodin mRNA; reduced C3aR mRNA and PLA2R mRNA; and improved podocyte viability, with Moshen Formula+C3aR antagonist group demonstrating the most pronounced effects (P<0.01). Conclusion: Moshen Formula may protect podocytes by regulating the C3a/C3aR pathway, downregulating PLA2R expression, stabilizing the podocyte cytoskeleton, and improving podocyte viability.

Key words：idiopathic membranous nephropathy; Moshen Formula; podocytes; C3a/C3aR pathway

发布时间：2026-03-28

点击量：375