Erratum to:J Huazhong Univ Sci Technol[Med Sci]36(4):548–553,2016 https://doi.org/10.1007/s11596-016-1623-6 In the originally published article(https://doi.org/10.1007/s11596-016-1623-6),the immunofluorescence images...Erratum to:J Huazhong Univ Sci Technol[Med Sci]36(4):548–553,2016 https://doi.org/10.1007/s11596-016-1623-6 In the originally published article(https://doi.org/10.1007/s11596-016-1623-6),the immunofluorescence images in shRNA group in Fig.3 were accidentally used rather than the final,formal experiments.To retain consistency,the entire Fig.3 is replaced here with original images of the experiments.The authors declare that this correction will not affect the conclusion of the study.展开更多
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
文摘Erratum to:J Huazhong Univ Sci Technol[Med Sci]36(4):548–553,2016 https://doi.org/10.1007/s11596-016-1623-6 In the originally published article(https://doi.org/10.1007/s11596-016-1623-6),the immunofluorescence images in shRNA group in Fig.3 were accidentally used rather than the final,formal experiments.To retain consistency,the entire Fig.3 is replaced here with original images of the experiments.The authors declare that this correction will not affect the conclusion of the study.
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.
