Astaxanthin improves HK-2 cell fibrosis by regulating mitochondrial autophagy
Objective To investigate the mechanism of astaxanthin(AST)in improving transforming growth factorβ1(TGF-β1)induced fibrosis in human renal tubular epithelial cells(HK-2).Methods HK-2 cells were divided into control group,TGF-β1 group,TGF-β1+20 μg/ml AST group,and TGF-β1+40 μg/ml AST group.Cell viability was assessed by CCK-8,and mitochondrial membrane potential level was detected by mitochondrial membrane potential detection kit.The mRNA expressions of α-smooth muscle actin(α-SMA),fibronectin(FN)were detceted by quan-titative real time polymerase chain reaction(qRT-PCR).The protein expressions of α-SMA,FN,microtubule-asso-ciated protein light chain 3(LC3)-Ⅱ/Ⅰ,P62,PINK1,and parkin were detected by Western blot.Results The mRNA,protein expressions of α-SMA,FN in TGF-βi group were higher than those of control group;and cell viability,mit-ochondrial membrane potential level were lower than those of control group(all P＜0.05).After treatment with 20μg/ml or 40 μg/ml AST in the TGF-β1 group;the mRNA,protein expressions of α-SMA,FN were significantly de-creased;while cell viability,mitochondrial membrane potential level were significantly increased(all P＜0.05).The protein expressions of LC3-Ⅱ/Ⅰ,parkinl,and PINK1 were higher than those of control group,and the protein ex-pression of P62 was lower than that of control group(all P＜0.05).Compared to the TGF-β1 group,the protein ex-pressions of LC3-Ⅱ/Ⅰ,parkinl,and PINK1 were significantly decreased,and the protein expression of P62 was sig-nificantly increased in the TGF-β1+20 μg/ml AST group and TGF-β1+40 μg/ml AST group(all P＜0.05).Con-clusions AST can alleviate TGF-β1-induced fibrosis in HK-2 cells by regulating mitophagy.
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