Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells via Partially Inhibiting Autophagy and ERK Signaling Pathway

Over-expression of angiotensin II (Ang II) is an important reason for the development of chronic kidney disease. Calycosin is the active component of traditional Chinese medicine astragali radix. The present work aims to explore whether calycosin could affect the growth and apoptosis ability of the Ang II treated glomerular mesangial cells and the underlying mechanism. Human glomerular mesangial cells (GMCs) were cultured and treated by Ang II and 0, 0.1, 1, or 10 µM calycosin, and the viability and proliferation of the cells were determined by methyl thiazolyl tetrazolium (MTT) and 5-ethynil-2′-deoxyuridine (EdU) staining; moreover, the apoptosis of the cells was examined by flow cytometry assay; furthermore, the expression levels of extracellular signal-regulated kinase (ERK), p-ERK, anti-apoptotic factor Bcl-2, as well as pro-apoptotic factor Bax have been examined by Western blot (WB) methods; finally, the expression of autophagic markers in each group was examined by WB and immunocytochemistry methods. We found that Ang II increased viability and proliferation, meanwhile inhibited apoptosis of the GMCs; furthermore, 1 and 10 µM calycosin significantly inhibited the growth and promoted the apoptosis of the GMCs treated by Ang II; moreover, calycosin also inhibited ERK signaling in mesangial cells activated by Ang II treatment; Finally, calycosin could inhibit Ang II induced autophagy of GMCs in a dose-dependent manner. In conclusion, calycosin may alleviate Ang II-induced pro-proliferative and anti-apoptotic effects on glomerular mesangial cells at least partially via inhibiting autophagy and ERK signaling pathway, suggesting that calycosin may function as a potential alternative medication for the management of chronic kidney diseases.