황금탕의 족돌기세포에서의 EMT 억제 효능

• Published in: 동의생리병리학회지 Vol. 34; no. 2; pp. 61 - 66
• Main Authors: 신상우(Sang Woo Shin), 정한솔(Han-Sol Jeong)
• Format: Journal Article
• Language: Korean
• Published: 한의병리학회 2020
• Subjects: 한의학; mTOR; AMPK; Epithelial?mesenchymal transition; Kidney fibrosis; Epithelial-mesenchymal transition
• ISSN: 1738-7698; 2288-2529; 2283-2529
• DOI: 10.15188/kjopp.2020.04.34.2.61

Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells lose their characters and acquire the properties of mesenchymal cells. EMT has been reported to exert an essential role in embryonic development. Recently, EMT has emerged as a pivotal mechanism in the metastasis of cancer and the fibrosis of chronic diseases. In particular, EMT is drawing attention as a mechanism of renal fibrosis in chronic kidney diseases such as diabetic nephropathy. In this study, we developed an EMT model by treating TGF-β1 on the podocytes, which play a key role in the renal glomerular filtration. This study explored the effects of Hwanggeum-tang (HGT) recorded in Dongeuibogam as being able to be used for the treatment of Sogal whose concept had been applied to Diabetes Mellitus (DM), on the TGF-β1-induced podocyte EMT. HGT suppressed the expression of vimentin and α-SMA, the EMT marker, in the human podocytes stimulated by TGF-β1. However, HGT increased the expression of ZO-1 and nephrin. Interestingly, HGT selectively inhibited the mTOR pathway rather than the classical Smad pathway. HGT also activated the AMPK signaling. HGT's inhibitory effect on the podocyte EMT through regulation of the mTOR pathway was achieved through the activation of AMPK, which was confirmed by comparison with cells treated with compound C (CC), an inhibitor of AMPK signaling. In conclusion, HGT can be applied to the renal fibrosis by preventing TGF-β1-induced EMT of podocytes through AMPK activation and mTOR inhibition.