| Objective: Acute liver failure with high mortality is still one of the clinical critically ill,in addition to artificial liver replacement therapy,liver transplantation,the lack of clinical treatment of special effects drugs,explore the clinical treatment of drugs is necessary.G-Rg1 was effective in the treatment of acute liver failure in mice,and may be related to anti-hepatocyte apoptosis and anti-inflammatory effect,but the specific mechanism of G-Rg1,the target are still unclear,Therefore,we establishment acute liver failure model induced by carbon tetrachloride(CCl4).To investigate the the mechanism of ginsenoside Rg1(G-Rg1)on acute liver failure model induced by carbon tetachloride(CCl4).Methods: Forty healthy,adult,male C57/BL mice were divided equally randomly into the control group(NS),G-Rg1 blank control(G-Rg1)group,CCl4 model(CCl4)group,G-Rg1 prevent(CCl4+G-Rg1)group.All mice were sacrificed to collect blood and liver specimens after twelve hours intraperitoneal injection.Serum alanine aminotransferase(ALT),serum aspartate aminotransferase(AST)and total bilirubin(TBil)were detected.Histological examination was detected by hematoxylin-eosin staining.The expression of glucose-regulated protein(GRP78),C/EBP homologousprotein(CHOP)were detected by real-time PCR.The protein expression of GRP78,CHOP,caspase12 and caspase3 were detected by western blot.The GRP78 and caspase3 were detected by immunohistochemistry.Apoptosis was detected using terminal transferase d UTP nick end labeling.Results: 1.The CCl4 +G-Rg1 prevent group show remarkably alleviate of tissue necrosis than the CCl4 group.2.The levels of serum ALT,AST and TBil in CCl4 +G-Rg1 group were significantly reduced as compared with those in CCl4 group.The ALT of NS group,G-Rg1 group,CCl4 group and CCl4 +G-Rg1 group were(50.12±9.25)U/L、(40.48±6.38)U/L、(980.66±110.29)U/L、(691.30±108.06)U/L;The AST of NS group,G-Rg1 group,CCl4 group and CCl4+G-Rg1 group were(9.69±2.78)U/L 、(9.40±3.84)U/L 、(319.44±89.32)U/L 、(195.40±15.41)U/L;The TBil of NS group,G-Rg1 group,CCl4 group and CCl4 +G-Rg1 group were(0.46±0.13)mg/d L 、(0.48±0.08)mg/d L 、(1.56±0.12)mg/d L、(1.09±0.11)mg/d L。3.The relative m RNA exspression of GRP78 and CHOP were significantly lower in CCl4 +G-Rg1 group than CCl4 group(F=34.4、F=44.1,P<0.05).4.The protein exspression of caspase3,GRP78,caspase12,CHOP were significantly lower in CCl4 +G-Rg1 group than CCl4 group(F=270.58、F=34.73、F=92.38、F=31.63,P<0.05).5.The expression of GRP78 and caspase3 was detected by immunohistochemistry.The results of light microscopy showed that the CCl4 group had a significant increase in the cytoplasmic granules.CCl4 + G-Rg1 group was decreased than CCl4 group cytoplasmic brown particles.6.The CCl4+G-Rg1 group showed remarkably less liver brown stain than CCl4 group,the indicating G-Rg1 prevent treatment can relieve liver apoptosis(F=330.9,P<0.05).Conclusion: G-Rg1 prophylaxis can reduce hepatocyte necrosis and apoptosis in acute liver failure(ALF)induced by CCl4.Maybe through reduce liver endoplasmic reticulum stress to relieve hepatocyte apoptosis.The results of this study suggests that G-Rg1 may inhibit liver inflammation and liver cell apoptosis in liver function for protection by the action of a plurality of targets. |
