XU Bo, WU Wei-nan, LI Chuan-jia, et al. Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(23): 139-143.
XU Bo, WU Wei-nan, LI Chuan-jia, et al. Protection Mechanism of Total Flavones from Hemerocallis Fulva on Alcohol-induced Liver Injury in Mice[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(23): 139-143. DOI: 10.13422/j.cnki.syfjx.2016230139.
Objective: To study the protection effect of total flavones from the hemerocallis fulva (TFHF) on alcohol-induced liver injury in mice and explore their possible pharmacological mechanisms. Method: A total of 60 mice were randomly divided into normal group
model group
bifendate group and TFHF low dose
middle dose
and high dose groups. Acute hepatic injury models were established by once gavage administration of alcohol. Levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum
as well as sup eroxide dismutase (SOD)
malondialdehyde (MDA)
glutathione peroxidase (GPX) and glutathione (GSH) levels in liver tissues were assayed and compared. The pathological changes in liver tissues were observed
and the expression levels of Bcl-2 and Bax were detected by Western blot. Result: As compared with the model group
TFHF could significantly reduce serum ALT and AST levels (P<0.05)
decrease the MDA content in liver tissues and increase the activities of SOD
GSH and GPX(P<0.05
P<0.01). Pathological examination showed that as compared with the model group
TFHF middle dose group and high dose group could significantly alleviate the liver cell degeneration and necrosis
and improve the pathological changes of hepatic tissues. Western blot results showed that the protein expression level of Bcl-2 was significantly increased in TFHF groups (P<0.05
P<0.01)
whereas the protein expression of Bax was decreased and Bax/Bcl-2 was also decreased (P<0.05
P<0.01). Conclusion: TFHF may have a significant protection effect on alcohol-induced liver injury in mice
and the mechanism may be associated with its antioxidation effect and regulating the expression levels of Bcl-2 and Bax.