Objective:To investigate the effect of apigenin on carbon tetrachloride(CCl_(4))-induced liver fibrosis and elucidate the underlying mechanisms.Methods:A mouse model of CCl_(4)-induced liver fibrosis was used to evalu...Objective:To investigate the effect of apigenin on carbon tetrachloride(CCl_(4))-induced liver fibrosis and elucidate the underlying mechanisms.Methods:A mouse model of CCl_(4)-induced liver fibrosis was used to evaluate the effects of apigenin.Liver function was assessed using biochemical tests,and inflammation-associated markers,including interleukin-1 beta(IL-1β),IL-6,IL-10,and tumor necrosis factor-alpha(TNF-α),were determined by enzyme-linked immunosorbent assay(ELISA).H&E staining,Sirius Red staining,and collagen immunohistochemistry were also conducted.In addition,antioxidant enzyme activity and the underlying mechanisms of hepatoprotective effects of apigenin were examined.Results:CCl_(4)administration induced hepatic stellate cell activation and liver fibrogenesis in mice.Apigenin treatment markedly decreased liver injury markers,inflammation,oxidative stress,and collagen deposition,mitigating CCl_(4)-induced liver fibrosis.Furthermore,it significantly suppressed the activation of the phosphoinositide 3-kinase/protein kinase B/glycogen synthase kinase 3 beta(PI3K/AKT/GSK3β)pathway by reducing the ratios of p-PI3K/PI3K,p-AKT/AKT,and p-GSK3β/GSK3βin liver tissue.Conclusions:Apigenin ameliorates CCl_(4)-induced liver fibrosis in mice,likely through the inhibition of the PI3K/AKT/GSK3βsignaling pathway.These findings suggest that apigenin may have therapeutic potential for treating liver fibrosis.展开更多
基金supported by the grant from Henan Province Science and Technology Research Project(Project No:242102310250,222102310373)Key Research Project Program of Higher Education Institutions in Henan Province(NO 24A32006,22B360003)Medical Science and Technology Tackling Program of Henan Province(NO LHGJ20230677).
文摘Objective:To investigate the effect of apigenin on carbon tetrachloride(CCl_(4))-induced liver fibrosis and elucidate the underlying mechanisms.Methods:A mouse model of CCl_(4)-induced liver fibrosis was used to evaluate the effects of apigenin.Liver function was assessed using biochemical tests,and inflammation-associated markers,including interleukin-1 beta(IL-1β),IL-6,IL-10,and tumor necrosis factor-alpha(TNF-α),were determined by enzyme-linked immunosorbent assay(ELISA).H&E staining,Sirius Red staining,and collagen immunohistochemistry were also conducted.In addition,antioxidant enzyme activity and the underlying mechanisms of hepatoprotective effects of apigenin were examined.Results:CCl_(4)administration induced hepatic stellate cell activation and liver fibrogenesis in mice.Apigenin treatment markedly decreased liver injury markers,inflammation,oxidative stress,and collagen deposition,mitigating CCl_(4)-induced liver fibrosis.Furthermore,it significantly suppressed the activation of the phosphoinositide 3-kinase/protein kinase B/glycogen synthase kinase 3 beta(PI3K/AKT/GSK3β)pathway by reducing the ratios of p-PI3K/PI3K,p-AKT/AKT,and p-GSK3β/GSK3βin liver tissue.Conclusions:Apigenin ameliorates CCl_(4)-induced liver fibrosis in mice,likely through the inhibition of the PI3K/AKT/GSK3βsignaling pathway.These findings suggest that apigenin may have therapeutic potential for treating liver fibrosis.
