Effect of WeiJia on carbon tetrachloride induced chronic liver injury

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:lzy19900924
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AIM:To study the effect of WeiJia on chronic liver injuryusing carbon tetrachloride(CCl_4)induced liver injuryanimal model.METHODS:Wistar rats weighing 180-220g were ran-domly divided into three groups:normal control group(Group A),CCl_4 induced liver injury control group(GroupB)and CCl_4 induction with WeiJia treatment group(GroupC).Each group consisted of 14 rats.Liver damage andfibrosis was induced by subcutaneous injection with 40%CCl_4 in olive oil at 3 mL/kg body weight twice a week foreight weeks for Groups B and C rats whereas olive oilwas used for Group A rats.Starting from the third week,Group C rats also received daily intraperitoneal injectionof WeiJia at a dose of 1.25 μg/kg body weight.Animalswere sacrificed at the fifth week(4 male,3 female),andeighth week(4 male,3 female)respectively.Degree offibrosis were measured and serological markers for liverfibrosis and function including hyaluronic acid(HA),typeIV collagen(CIV),γ-glutamyl transferase(γ-GT),alanineaminotransferase(ALT)and aspartate aminotransferase(AST)were determined.Alpha smooth muscle actin (α-SMA)and proliferating cell nuclear antigen(PCNA)immunohistochemistry were also performed.RESULTS:CCl_4 induction led to the damage of liver anddevelopment of fibrosis in Group B and Group C ratswhen compared to Group A rats.The treatment of WeiJiain Group C rats could reduce the fibrosis condition sig-nificantly compared to Group B rats.The effect could beobserved after three weeks of treatment and was moreobvious after eight weeks of treatment.Serum HA,CIV,ALT,AST and γ-GT levels after eight weeks of treatmentfor Group C rats were 58±22 μg/L(P<0.01),57±21 μg/L(P<0.01),47±10 U/L(P<0.01),139±13 U/L(P<0.05)and 52±21 U/L(P>0.05)respectively,similar to normalcontrol group(Group A),but significantly different fromCCl_4 induced liver injury control group(Group B).An in-crease in PCNA and decrease in α-SMA expression levelwas also observed.CONCLUSION:WeiJia could improve liver function andreduce liver fibrosis which might be through the inhibi-tion of stellate cell activity. AIM: To study the effect of WeiJia on chronic liver injury using carbon tetrachloride (CCl_4) induced liver injury animal model. METHODS: Wistar rats weighing 180-220 g were ran-domly divided into three groups: normal control group (Group A), CCl_4 induced liver injury control group (GroupB) and CCl_4 induction with WeiJia treatment group (GroupC). Each group consisted of 14 rats. Liver damage and fibrosis was induced by subcutaneous injection with 40% CCl_4 in olive oil at 3 mL / kg body weight twice a week foreight weeks for Groups B and C rats where olive oil was used for Group A rats. Starting from the third week, Group C rats also received daily intraperitoneal injection of WeiJia at a dose of 1.25 μg / kg body weight. Animal sacrifices for the fifth week (4 (4 male, 3 female) respectively. Degree of offibrosis were measured and serological markers for liver fibrosis and function including hyaluronic acid (HA), type IV collagen (CIV), γ-glutamyl transferase (γ-GT) , alanineaminotransfe RESULTS: CCl_4 induction led to the damage of liver and development of fibrosis in Group (ALA) and aspartate aminotransferase (AST) were determined. B and Group C rats when compared to Group A rats. The treatment of WeiJiain Group C rats could reduce the fibrosis condition sig-nificantly compared to Group B rats. The effect could beobserved after three weeks of treatment and was moreobvious after eight weeks of treatment. Serum HA, CIV, ALT, AST and γ-GT levels after eight weeks of treatment for Group C were 58 ± 22 μg / L (P <0.01), 57 ± 21 μg / L Similar to normal control group (Group A), but significantly different fromCCl_4-induced liver injury control (P <0.05) and 52 ± 21 U / L group (Group B). An in-crease in PCNA and decrease in α-SMA expression level was also observed. CONCLUSION: WeiJia could improve liver function andreduce liver fibrosis which might be through the inhibition of stellate cell activity.
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