OBJECTIVE To study the protection effects and mechanisms of NYG-1 on CCl4-induced acute liver injury.METHODS Acute liver injury model of rats was established by using CCl4.48 male SPF SD rats were weighed and randomly divided into six groups with 8 in each group,normal group,model group,positive control group(silibinin),low-,medium-and high-dose NYG-1 group.Silibinin was given orally to rats in the positive control group,NYG-1(high-,medium-and low-dose)was given orally in the high-,medium-and low-dose NYG-1group,respectively.Those rats were administered appropriately according to the group once daily for seven consecutive days.On the seventh day,rats were treated with 10% CCl4(10mL·kg-1 of0.1% CCl4 solution in olive oil)intraperitoneally injecting(ip)to induce acute liver injury,except the normal group.At 16 h after CCl4 treatment,rats were weighed,then anaesthed with ether,the blood and liver were collected.Serum ALT,AST,LDH and ALP were measured.MDA content and SOD activity in liver homogenate were detected.The histopathological changes of liver were observed by H&E staining.RESULTS Acute liver injury model was established successfully in rats by intraperitoneally injecting CCl4.Pretreatment with medium and high dose NYG-1 decreased the increase of ALT,AST and MDA induced by CCl4,but it had no influence on serum LDH,ALP level and SOD activity in the liver homogenate.CONCLUSION The obtained results suggest that oral administration of NYG-1 hasve the protective effects against CCl4-induced acute hepatic injury in rats,Its mechanism may be related to antioxidant-like action. OBJECTIVE To study the protection effects and mechanisms of NYG-1 on CCl4-induced acute liver injury. METHODS Acute liver injury model of rats was established by using CCl4.48 male SPF SD rats were weighed and randomly divided into six groups with 8 in each group, normal group, model group, positive control group (silibinin), low-, medium- and high-dose NYG-1 group. Limbinin was given orally to rats in the positive control group, NYG- and low-dose) was given orally in the high-, medium- and low-dose NYG-1 group, respectively. Ten rats were administered appropriately according to the group once daily for seven consecutive days. On the seventh day, rats were treated with 10% CCl4 (10 mL · kg-1 of 0.1% CCl4 solution in olive oil) intraperitoneally injected (ip) to induce acute liver injury, except the normal group. At 16 h after CCl4 treatment, rats were weighed, then anaesthed with ether , the blood and liver were collected. Serum ALT, AST, LDH and ALP were measured. MDA content and SOD activity in liver homogenate were detected by histopathological changes of liver were observed by H & E staining. RESULTS Acute liver injury model was established successfully in rats by intraperitoneally injecting CCl4.Pretreatment with medium and high dose NYG-1 decreased the ALT, AST and MDA induced by CCl4, but it had no influence on serum LDH, ALP level and SOD activity in the liver homogenate. CONCLUSION The resulting results suggest that oral administration of NYG-1 has had the protective effects against CCl4-induced acute hepatic injury in rats, Its mechanism may be related to antioxidant-like action.