Abstract: Objective　To explore the prevention and mechanism of cannabidiol (CBD) on carbon tetrachloride (CCl4)-induced acute liver injury in mice. Methods　Forty-two C57BL/6J male mice aged 6-8 weeks were divided into 5 groups according to the random number table method: control group (n=9), model group (n=9), CBD control group (n=9), glutathione (GSH) intervention group (n=6) and CBD intervention group (n=9). The CBD control group, GSH intervention group and CBD intervention group were intraperitoneally injected with CBD 5 mg/kg, GSH 200 mg/kg and CBD 5 mg/kg respectively. The control group and model group were injected with the same dose of normal saline. Two hours later, the model group, GSH intervention group and CBD intervention group were intraperitoneally injected with 20% CCl4 olive oil 5 mL/kg to establish the acute liver injury model. After 24 h, the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected. HE staining was used to observe the pathological changes of mouse liver tissue. The activities of superoxide dismutase (SOD), malondialdehyde (MDA) and GSH were detected by liver tissue homogenate method. PPAR-γ and COX-2 protein expression levels in liver tissue were detected by Western blot assay. Results　Compared with the control group, the model group had severe cell damage and necrosis, ALT, AST, MDA and COX-2 levels were significantly increased in the model group (P＜0.05), and the SOD, GSH and PPAR-γ levels were significantly reduced (P＜0.05). Compared with the model group, liver pathological damages significantly reduced in the GSH intervention group and CBD intervention group, and ALT, AST, MDA and COX-2 levels were significantly reduced (P＜0.05), whereas SOD, GSH and PPAR-γ levels were significantly increased (P＜0.05). Conclusion　CBD can prevent CCl4 induced the acute liver injury in mice, which may be related to the activation of PPAR-γ, the inhibition of COX-2 expression and anti-inflammatory and antioxidant effects.

Key words: cannabidiol, carbon tetrachloride, PPAR gammacy, clooxygenase 2, chemical and drug induced liver injury, oxidative stress, acute liver injury