Astragaloside IV Attenuates Complement Membranous Attack Complex Induced Podocyte Injury Through the MAPK Pathway
Astragaloside IV Attenuates Complement Membranous Attack Complex Induced Podocyte Injury Through the MAPK Pathway
复制标题
DOI：
10.1002/ptr.3656
复制
发表时间：
2012-06-01
影响因子：
7.2
通讯作者：
Wang, Lin
中科院分区：
文献类型：
--
作者：
Zheng, Rong;Deng, Yueyi;Wang, Lin
膜性肾病（MN）是成人特发性肾病综合征的最常见原因，已知其原因是由于肾小球中足细胞的损伤。黄芪在我国长期用于治疗MN患者。黄芪对MN患者蛋白尿的有益作用已被充分证明。然而，黄芪缓解MN的机制仍不完全清楚。因此，本研究采用补体膜攻击复合物诱导的足细胞损伤模型，探讨黄芪治疗MN的机制。我们发现，补体膜攻击复合物可以增加足细胞释放乳酸脱氢酶（LDH），黄芪甲苷IV（AS-IV）可以抑制足细胞释放LDH的时间和剂量依赖性模式。此外，AS-IV恢复足细胞形态和细胞骨架的补体膜攻击复合物引起的损失。AS-IV还能降低补体膜攻击复合物诱导的JNK和ERK 1/2的磷酸化。黄芪治疗MN的机制可能与其通过调节细胞骨架和丝裂原活化蛋白激酶减轻足细胞损伤有关。版权所有（c）2011年约翰威利父子有限公司
Membranous nephropathy (MN) is the most common cause of idiopathic nephrotic syndrome in adults and the cause is known to be due to the injury of podocytes located in the glomeruli. Astragalus membranaceus has been used for the treatment of patients with MN in China for a long time. The beneficial effect of Astragalus membranaceus on proteinuria of patients with MN has been well documented. However, the mechanism of astragalus membranaceu in alleviation of MN is still not completely understood. Therefore, in the current study, we employed a podocyte injury model induced by complement membranous attack complex to examine the mechanism of astragalus membraneceus in the treatment of MN. We found that complement membranous attack complex could increase lactate dehydrogenase (LDH) release from podocytes and astragaloside IV (AS-IV) could prevent LDH release from podocytes in a time- and dose-dependent pattern. Moreover, AS-IV restored podocyte morphology and cytoskeleton loss induced by complement membranous attack complex. Furthermore, AS-IV was able to reduce phosphorylation of JNK and ERK1/2 induced by complement membranous attack complex. In conclusion, the mechanism of Astragalus membranaceus in the treatment of MN may be related to its attenuation of podocyte injury through regulation of cytoskeleton and mitogen activated protein kinase. Copyright (c) 2011 John Wiley & Sons, Ltd.