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目的:观察山茱萸总苷(TGCO)对刀豆蛋白A(Con A)诱导的小鼠急性免疫性肝损伤的保护作用,并探讨其作用机制。方法:将60只C57BL小鼠随机分为正常组、模型组、阳性对照组、TGCOH组、TGCOM组、TGCOL组,每组10只;正常组和模型组以0.2 mL/10 g生理盐水灌胃,阳性对照组给予联苯双酯150 mg/kg灌胃,TGCOH组、TGCOM组、TGCOL组给予TGCO溶液460、230、115 mg/kg灌胃,1次/d,连续14 d。末次给药后2 h,正常组尾静脉注射生理盐水,其余各组尾静脉注射Con A制备小鼠免疫性肝损伤模型。8 h后称重,处死小鼠,计算各组小鼠肝、脾系数并取肝组织进行HE染色观察病理学变化;检测各组小鼠血清丙氨酸氨基转移酶(ALT)和门冬氨酸氨基转移酶(AST)水平;检测肝组织肿瘤坏死因子α(TNF-α)、γ干扰素(IFN-γ)、白介素1(IL-1)、白介素6(IL-6)、超氧化物歧化酶(SOD)、鸟氨酸氨基甲酰转移酶(OTC)含量。结果:与模型组比较,各浓度TGCO组小鼠肝组织的病变程度较轻,血清ALT、AST水平及肝组织中TNF-α、IFN-γ、IL-1、IL-6、OTC含量均降低,肝组织中SOD水平升高(P<0.05)。结论:TGCO对免疫性肝损伤小鼠具有一定的保护作用,其作用机制可能与降低转氨酶,提高抗氧化能力和抑制TNF-α、IFN-r、IL-1、IL-6生成有关。
Objective: To observe the protective effect of total glucosides of Cornus officinalis (TCO) on acute immunity-induced liver injury induced by Con A in mice and to explore its mechanism. Methods: 60 C57BL mice were randomly divided into normal group, model group, positive control group, TGCOH group, TGCOM group and TGCOL group, with 10 rats in each group. Normal group and model group were treated with 0.2 mL / 10 g normal saline , The positive control group was given bifendate 150 mg / kg gavage, TGCOH group, TGCOM group, TGCOL group were given TGCO solution 460,230,115 mg / kg gavage once a day for 14 days. At 2 h after the last administration, saline was injected into the caudal vein in the normal group, and mice in the other groups were injected with Con A to establish immunological liver injury model. After 8 h, the mice were weighed and sacrificed. The liver and spleen indexes of the mice in each group were calculated and the liver tissues were taken for HE staining to observe the pathological changes. Serum alanine aminotransferase (ALT) and aspartate The levels of tumor necrosis factor alpha (TNF-α), interferon-γ (IFN-γ), interleukin 1 (IL-1), interleukin 6 (IL-6), superoxide Dismutase (SOD), ornithine carbamoyltransferase (OTC) content. Results: Compared with the model group, the pathological changes of liver tissue of mice in TGCO group at each concentration were lighter and the levels of ALT and AST and the content of TNF-α, IFN-γ, IL-1, IL-6 and OTC , SOD level in liver tissue increased (P <0.05). CONCLUSION: TGCO can protect mice with autoimmune liver injury and its mechanism may be related to the reduction of transaminase, anti-oxidation ability and the inhibition of TNF-α, IFN-γ, IL-1 and IL-6 production.