Xanthohumol Inhibits TGF-β1-Induced Cardiac Fibroblasts Activation via Mediating PTEN/Akt/mTOR Signaling Pathway

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Abstract
Background: Xanthohumol (Xn) is the most abundant prenylated flavonoid in Hops (Humulus lupulus L.), and exhibits a range of pharmacological activities. This study aimed to investigate the effect of Xn on TGF-β 1-induced cardiac fibroblasts activation and elucidate the underlying mechanism. Materials and Methods: The cellTiter 96® AQueous one solution cell proliferation assay kit was adopted to determine the cell viability of cardiac fibroblasts, and the proliferation was detected through 5-ethynyl-2ʹ-deoxyuridine (EdU) incorporation assay. The α-SMA protein expression was measured by using immunofluorescence and Western blotting. Western blotting was conducted to test the protein expressions of collagen I and III, PTEN, p-Akt, Akt, p-mTOR, mTOR, p-Smad3, Smad3 and GAPDH. The mRNA levels of α-SMA, collagen I and III were determined by quantitative real-time polymerase chain reaction (PCR). Results: Xn inhibited the TGF-β 1-induced proliferation, differentiation and collagen overproduction of cardiac fibroblasts. TGF-β 1 induced the down-regulated PTEN expression, Akt and mTOR phosphorylation. These effects of TGF-β 1 were suppressed by Xn, while blocking of PTEN reduced Xn-mediated inhibitory effect on cardiac fibroblasts activation induced by TGF-β 1. Conclusion: Xn inhibits TGF-β 1-induced cardiac fibroblasts activation via mediating PTEN/Akt/mTOR signaling pathway.

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