Emodin-induced autophagic cell death hinders epithelial-mesenchymal transition via regulation of BMP-7/TGF-ß1 in renal fibrosis.

ABSTRACT

We aim to explore the effects of emodin and its mechanisms on renal fibrosis (RF). We firstly modeled adriamycin-induced rat RF with unilateral nephrectomy. In vivo and in vitro pharmacological experiments were performed in this study. The presence of collagen deposition was detected by Masson staining. To verify whether emodin attenuates RF by monitoring autophagy, the immunohistochemistry staining for autophagy protein LC3B was performed. We conducted western blot to detect the expression of the autophagy-related proteins in EMT in vitro model after treating with emotin and BMP-7. In vivo, we demonstrated that emodin could improve renal dysfunction and decrease pathological damage of the kidney by activation of autophagy and inhibition of EMT. Upregulation of BMP-7 was recorded in the RF rats subjected to emodin treatment. In vitro studies, emodin has the capacity of reversing EMT and activating autophagy, and emodin could regulate the expression of BMP-7. The results revealed that the attenuation of EMT by emodin could be blocked after the inhibition of BMP-7 and suppression of autophagy. Our findings demonstrated that emodin alleviates EMT during RF by actuating autophagy through BMP-7, suggesting a role of BMP-7 in RF treatment and prevention.