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目的通过观察表没食子儿茶素没食子酸酯(EGCG)对ConA诱导的急性肝损伤小鼠肝组织中NF-κB及ICAM-1表达的影响,来探讨EGCG对小鼠的肝保护机制。方法 C57BL/6小鼠分成4组:对照组、EGCG对照组、ConA模型组,EGCG+ConA组。EGCG对照组及EGCG+ConA组小鼠给予EGCG口服(5 mg/kg)10 d后,予模型组小鼠静脉注射ConA(15 mg/kg)建造肝损伤模型,采血及留取肝组织,HE法检测肝组织病理变化,ELISA法检测NF-κB及ICAM-1的表达。结果 ConA模型组小鼠肝损伤明显,NF-κB及ICAM-1的表达明显增多,与对照组比较有显著性差异(P<0.05);EGCG治疗组肝损伤减轻且伴NF-κB及ICAM-1的表达下降,与模型组比较差异明显(P<0.05)。结论 EGCG对ConA诱导的免疫性肝损伤小鼠有保护作用,其机制可能与调节NF-κB及ICAM-1的表达有关。
OBJECTIVE: To investigate the effect of epigallocatechin-3-gallate (EGCG) on the expression of NF-κB and ICAM-1 in liver of ConA-induced acute liver injury mice. Methods C57BL / 6 mice were divided into 4 groups: control group, EGCG control group, ConA model group and EGCG + ConA group. EGCG control group and EGCG + ConA group mice were given EGCG orally (5 mg / kg) for 10 days, the model group mice were injected with ConA (15 mg / kg) to establish liver injury model, Pathological changes of liver were detected by ELISA, and the expressions of NF-κB and ICAM-1 were detected by ELISA. Results Compared with control group, the expression of NF-κB and ICAM-1 in ConA model group was significantly increased (P <0.05). The liver injury in EGCG group was relieved with NF-κB and ICAM- 1 expression decreased significantly compared with the model group (P <0.05). Conclusion EGCG can protect ConA-induced immune-induced liver injury in mice, and its mechanism may be related to the regulation of NF-κB and ICAM-1 expression.