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Aristolochic Acid I Aggravates Renal Injury by Activating the C3a/C3aR Complement System

Aristolochic Acid I Aggravates Renal Injury by Activating the C3a/C3aR Complement System

Jing Ye, Zhizhi Qian, Mei Xue, Yamin Liu, Sirui Zhu, Yu Li, Xiaoli Liu, Danhong Cai, Jia Rui, Liang Zhang

Toxicol Lett. 2019 Sep 15;312:118-124.

PMID: 31048001

Abstract:

Previous studies have reported that the complement system is unconventionally activated in many kinds of glomerulonephritis. Multiple complement components participate in the pathogenic process by triggering immune response or other intracellular signaling pathways. Here, we have investigated the role of C3a and its receptor C3aR in aristolochic acid nephropathy (AAN), which, is featured with progressive interstitial fibrosis. Over release of C3a and increased expression of C3aR parallels to the up-regulation of α-SMA and TGF-β1 in AAN, which appeared to promote epithelial-mesenchymal-transition (EMT). To identify the role of complement activation in AAN, we used an inhibitor of C3aR (C3aRA) to block the coupling of C3a to its receptor. Our results confirmed from decreased EMT, the protective effect of C3aRA in cell apoptosis and inflammatory response induced by aristolochic acid I. These results showed that C3a and its receptor C3aR played pathogenic roles in AAN, and renal tubular epithelial cells were potentially pivotal targets of complement activation that could cause pro-fibrotic effects.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP313677-A	Aristolochic acid I		313-67-7	Price

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