Objective: To investigate the protective effect of Zhizi Dahuang Tang (ZDT) on carbon tetrachloride (CCl4)-induced acute hepatic injury in mice. Method: A total of 72 KM mice were randomly divided into normal control group

model group

bifendate pill group

ZDT low-dose group

ZDT medium-dose group and ZDT high-dose group

with 12 mice in each group. Bifendate pill (0.2 g·kg-1) or different doses (6

12

24 g·kg-1) of ZDT were given to corresponding groups by gavage for consecutively 5 days. The same volume of saline was infused in normal control group and model group. All groups of mice were intraperitoneally (ip) injected with CCl4

except for normal control group. Mice were sacrificed to collect their blood and liver specimens. Serum alanine aminotransferase (ALT)

aspartate aminotransferase (AST)

liver superoxide dismutase (SOD) and malondialdehyde (MDA) were detected. Histological examination was performed using hematoxylin-eosin staining and light microscopy

and Bax

Bcl-2 and Cleaved-Caspase-3 were detected for apoptosis by using Western blot. Result: Compared with the normal group

the normal group showed significant increases in serum AST and ALT activities (P<0.05) and MDA content

decreases in SOD activity(P<0.05)

hepatocyte deformation and necrosis

up-regulations in Bax and Cleaved-Caspase-3 expressions and down-regulation of Bcl-2 expression; compared with the model group

ZDT groups showed significant decreases in serum ALT activity (P<0.05)

and ZDT medium and high-dose groups showed significant decreases in serum AST activity(P<0.05)

and all of the groups showed significant reduction in MDA content (P<0.05) and rise in SOD activity (P<0.05). According to hepatic tissue sections

all of the treatment groups showed alleviations in hepatocyte deformation and necrosis

particularly the high-dose group

and all of ZDT groups showed down-regualtions in hepatic tissue Bax

Cleaved-Caspase-3 expression

and up-regulation in Bcl-2. Conclusion: ZDT exhibits a protective effect on CCl4-induced hepatic injury by resisting anti-lipid peroxidation and suppressing the apoptosis of liver tissues.