Liquiritin inhibits TGF-β1-induced epithelial mesenchymal transition and extracellular matrix deposition in human renal proximal tubular epithelial cells by suppressing the MAPK signaling

BackgroundExcessive extracellular matrix (ECM) deposition leads to renal fibrosis, a typical hallmark of chronic kidney disease. Liquiritin is a flavonoid extracted from the rhizome part of Glycyrrhiza glabra and has anti-fibrotic and nephroprotective effects. However, its role and underlying mechanism in renal fibrosis remain unknown.MethodsHuman renal proximal tubular epithelial cells (HRPTEpiCs) were stimulated with 10 ng/mL TGF-& beta;1 to induce renal fibrosis models in vitro. The morphology of HRPTEpiCs was observed under a light microscope. CCK-8 was utilized to test cell viability. Immunofluorescence staining was conducted to measure & alpha;-SMA expression in HRPTEpiCs. RT-qPCR was used to assess relative mRNA expression. The protein levels of ECM markers, epithelial mesenchymal transition (EMT) markers, and MAPK signaling-related molecules in HRPTEpiCs were tested using western blotting.ResultsTGF-& beta;1-treated HRPTEpiCs showed a fibroblast-like morphology, and the morphology of HRPTEpiCs was restored by liquiritin. Liquiritin suppressed TGF-& beta;1-stimulated ECM deposition and EMT process in HRPTEpiCs. Additionally, liquiritin repressed TGF-& beta;1-induced MAPK signaling activation in HRPTEpiCs.ConclusionLiquiritin mitigates TGF-& beta;1-triggered EMT process and ECM deposition in HRPTEpiCs by inactivating MAPK signaling, thus preventing renal fibrosis.