Yiqihuoxue Formula Activates Autophagy and Offers Renoprotection in a Rat Model of Adenine-Induced Kidney Disease

Figure 7

Schematic diagram of the effect of the YQHX formula on the renal tubular cell damage induced by adenine. Adenine feeding induced a series of injury factors, including oxidative stress, inflammation response, cellular hypoxia, and DNA damage, which further caused cell apoptosis by eventually activating caspase-3 and induced cell fibrosis by initiating the TGF-β signaling pathway. TGF-β signaling contributes to the phenotypic conversion program of the epithelial-mesenchymal transition (EMT) by gaining mesenchymal features (including α-smooth muscle actin, interstitial matrix components type I collagen, and fibronectin). The effective components of the YQHX formula ameliorated the cell apoptosis by upregulating the Bcl-2 expression and sequentially reducing the caspase-3 expression. Meanwhile, the YQHX formula activated the autophagy pathway by increasing the levels of Beclin-1, ATG-5, and LC3-II, thereby degrading the substrate p62, misfolded proteins, and injured cell organelles. Mature TGF-β induced by injury factors was reduced by the autophagy pathway.