RESUMO
AIM:To investigate the effects of dexmedetomidine (DEX) on acute alcoholic hepatic injury in mice and to explore the possible mechanisms .METHODS:Kunming mice (n=50) were randomly divided into 5 groups (n=10):normal saline control (NS) group, acute alcoholic hepatic injury model (E) group, low-dose (10μg/kg) DEX (E+L) group, medium-dose (50 μg/kg) DEX (E+M) group and high-dose (100 μg/kg) DEX (E+H) group.The animals were sacrificed at 6 h after gavage of alcohol or normal saline .The levels of alanine aminotransferase ( ALT) , as-partate aminotransferase (AST), triglyceride (TG), malondialdehyde (MDA), glutathione (GSH) and superoxide dis-mutase ( SOD) were measured .The livers were removed for evaluation of histological characteristics and determining the content of tumor necrosis factor-α( TNF-α) amd interleukin-1β( IL-1β) in the liver tissues by ELISA .The expression levels of cytochrome P4502E1 (CYP2E1) and nuclear factor -κB (NF-κB) in the liver tissues were evaluated by Western blot.RESULTS:Compared with NS group, the levels of ALT, AST and TG were obviously increased in E group , which were obviously decreased in E +M and E+H groups.Compared with NS group, the levels of TNF-α, IL-1βand MDA were obviously increase in E group , which were obviously decreased in E +M and E+H groups.Compared with NS group, the activity of SOD and the content of GSH were obviously decreased in E group , which were obviously increased in E +M and E+H groups.Compared with NS group, the expression of CYP2E1 and NF-κB was obviously increase in E group , which was obviously decreased in E +M and E+H groups.Compared with NS group , ethanol induced marked liver histo- logical injury, which was less pronounced in E +M and E+H groups.CONCLUSION: DEX has a protective effect on mouse liver with acute alcoholic injury by the involvement in the processes of antioxidation and antiinflammation , and its mechanism may be associated with the inhibition of CYP 2E1 and NF-κB expression.
RESUMO
AIM:To investigate the effects of dexmedetomidine (DEX) on acute alcoholic hepatic injury in mice and to explore the possible mechanisms .METHODS:Kunming mice (n=50) were randomly divided into 5 groups (n=10):normal saline control (NS) group, acute alcoholic hepatic injury model (E) group, low-dose (10μg/kg) DEX (E+L) group, medium-dose (50 μg/kg) DEX (E+M) group and high-dose (100 μg/kg) DEX (E+H) group.The animals were sacrificed at 6 h after gavage of alcohol or normal saline .The levels of alanine aminotransferase ( ALT) , as-partate aminotransferase (AST), triglyceride (TG), malondialdehyde (MDA), glutathione (GSH) and superoxide dis-mutase ( SOD) were measured .The livers were removed for evaluation of histological characteristics and determining the content of tumor necrosis factor-α( TNF-α) amd interleukin-1β( IL-1β) in the liver tissues by ELISA .The expression levels of cytochrome P4502E1 (CYP2E1) and nuclear factor -κB (NF-κB) in the liver tissues were evaluated by Western blot.RESULTS:Compared with NS group, the levels of ALT, AST and TG were obviously increased in E group , which were obviously decreased in E +M and E+H groups.Compared with NS group, the levels of TNF-α, IL-1βand MDA were obviously increase in E group , which were obviously decreased in E +M and E+H groups.Compared with NS group, the activity of SOD and the content of GSH were obviously decreased in E group , which were obviously increased in E +M and E+H groups.Compared with NS group, the expression of CYP2E1 and NF-κB was obviously increase in E group , which was obviously decreased in E +M and E+H groups.Compared with NS group , ethanol induced marked liver histo- logical injury, which was less pronounced in E +M and E+H groups.CONCLUSION: DEX has a protective effect on mouse liver with acute alcoholic injury by the involvement in the processes of antioxidation and antiinflammation , and its mechanism may be associated with the inhibition of CYP 2E1 and NF-κB expression.
RESUMO
Objective To investigate the protective effects of polysaccharide from Radix Codonopsis Lanceolatae on acute alcoholic hepatic injury in mice.Methods The model of CCl4-induced acute hepatic injury was set up in mice, and then treated with polysaccharide from Radix Codonopsis Lanceolatae to observe the activities of ALT, AST and TG in serum and the levels of SOD, GSH and MDA in hepatic tissue and Observed the pathological changes in the liver of mice.Results Compared with model control group, the lance asiabell root polysaccharide liver injury in mice all dose groups in the activity of serum ALT(97.5 ± 22.12 U/L, 108.8 ± 22.15 U/L, 125.2 ± 19.68 U/Lvs. 152.3 ± 17.32 U/L), AST (72.5 ± 21.3 U/L, 89.2 ± 17.47 U/L, 104.3 ± 19.34 U/Lvs.1215 ± 22.31 U/L) and TG(0.75 ± 0.32 mmol/L, 0.80 ± 0.22 mmol/L, 0.96 ± 0.21 mmol/L vs.1.44 ± 0.23 mmol/L) reduce, can increase the liver damage the activity of SOD(215.6 ± 22.68 U/mg, 203.2 ± 22.18 U/mg, 186.2 ± 18.34 U/mgvs.164.3 ± 17.54 U/mg), GSH(17.74 ± 2.12μmol/g, 14.84 ± 1.12μmol/g, 13.93 ± 2.15μmol/gvs.12.23 ± 2.09μmol/g) in liver tissue of mice, decrease the activity of MDA(6.22 ± 2.12 nmol/mg, 6.22 ± 2.12 nmol/mg, 8.36 ± 1.84 nmol/mgvs.9.35 ± 1.68 nmol/mg) in liver tissue, showing significant differences (P<0.05), and there was certain dose dependent, and can improve the pathological injury of liver tissue.Conclusion Polysaccharide from Radix Codonopsis Lanceolatae had protective effects on acute liver induced by acute alcoholic hepatic injury in mice.