WANG Zhongyi, ZHANG Zhijie, YAO Yale, CHEN Guowen, MA Xiaoyan, AN Zhixia, FAN Biyue, QIU Shantong, WANG Meng. Effects of FSLE on oxidative stress and inflammatory factors in APAP-induced liver injury miceJ. Journal of Gansu Agricultural University, 2024, 59(4): 1-8. DOI: 10.13432/j.cnki.jgsau.2024.04.001
Citation: WANG Zhongyi, ZHANG Zhijie, YAO Yale, CHEN Guowen, MA Xiaoyan, AN Zhixia, FAN Biyue, QIU Shantong, WANG Meng. Effects of FSLE on oxidative stress and inflammatory factors in APAP-induced liver injury miceJ. Journal of Gansu Agricultural University, 2024, 59(4): 1-8. DOI: 10.13432/j.cnki.jgsau.2024.04.001

Effects of FSLE on oxidative stress and inflammatory factors in APAP-induced liver injury mice

  • 【Objective】 This study aimed to investigate the impact of the ethanolic extract of Forsythia leaves(FSLE) on acetaminophen(APAP)-induced liver injury and its underlying mechanism.【Method】 Forty-eight Kunming mice were randomly assigned to six groups: the blank control group(NC),APAP liver injury model group(LD),FSLE control group(FSLE),and high,medium,and low doses of FSLE treatment groups(HFSLE+LD,MFSLE+LD,and LFSLE+LD),with eight mice in each group. The liver injury model was established,and drug administration took place. The levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),superoxide dismutase(SOD) activity,glutathione(GSH),malondialdehyde(MDA),and hydrogen peroxide(H2O2) were assessed in each group of mice. Liver histopathological changes were observed through hematoxylin-eosin staining(HE). TRAF2,NF-κB p65mRNA,and protein expression levels were measured,along with TNF-α,IL-1β,and IL-6 levels.【Result】 FSLE reduced ALT and AST activity,MDA,and H2O2 content,while increasing SOD activity and GSH content. It also ameliorated liver histopathology,decreased TRAF2 and NF-κB p65 mRNA and protein expression,and lowered TNF-α,IL-1β,and IL-6 levels in mice with liver injury.【Conclusion】 In conclusion,FSLE demonstrated hepatoprotective effects against APAP-induced liver injury by mitigating oxidative stress,modulating the TNF/NF-κB p65 signaling pathway,and suppressing the inflammatory response.
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