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目的探讨人参果花青素(ginseng fruit anthocyanins,GFA)对对乙酰氨基酚(acetaminophen,AP)致小鼠急性肝损伤的保护作用及其机制。方法建立AP诱导的肝损伤模型,观察GFA对肝损伤的保护作用。将ICR小鼠随机分为对照组、模型组(AP 250 mg/kg)和GFA低、高剂量(200、400 mg/kg)组。通过计算脏器指数,检测血清中的丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)及肝组织匀浆中的丙二醛(MDA)、谷胱甘肽(GSH)水平,结合肝组织切片来观察病理学变化。结果与模型组相比,GFA低、高剂量明显抑制了血清中ALT、AST和匀浆中MDA水平的升高,同时缓解了肝组织匀浆中GSH水平的降低(P<0.05);组织病理学HE和Hoechst 33258染色显示GFA可明显改善肝组织的坏死和凋亡,并且缩小了坏死区域,减轻了细胞炎性浸润;通过炎症因子诱导型一氧化氮合酶(i NOS)、环氧化酶-2(COX-2)免疫组织化学染色和硝化应激指标3-硝基络氨酸(3-NT)免疫荧光的表达,说明GFA能够抑制硝化应激和炎症反应。结论 GFA对AP诱导的急性肝损伤有一定的保护作用,其机制可能与其抗氧化作用、抑制硝化应激、减少炎症反应及抑制细胞凋亡有关。
Objective To investigate the protective effect of ginseng fruit anthocyanins (GFA) on acute liver injury induced by acetaminophen in mice and its mechanism. Methods The AP-induced liver injury model was established and the protective effect of GFA on liver injury was observed. The ICR mice were randomly divided into control group, model group (AP 250 mg / kg), low GFA and high dose (200 and 400 mg / kg) groups. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver homogenate were assayed for malondialdehyde (MDA), glutathione (GSH) , Combined with liver tissue sections to observe the pathological changes. Results Compared with the model group, low and high GFA significantly inhibited the increase of serum ALT, AST and the level of MDA in the homogenate, and alleviated the decrease of GSH in the liver homogenate (P <0.05) Neither histological HE nor Hoechst 33258 staining showed that GFA markedly ameliorates necrosis and apoptosis in liver tissue, reduces the necrotic area and reduces cellular inflammatory infiltration. It is also mediated by inflammatory factor-inducible nitric oxide synthase (iNOS), epoxidation Enzyme-2 (COX-2) immunohistochemical staining and nitration stress indicator 3-nitro-tyrosine (3-NT) immunofluorescence, indicating that GFA can inhibit nitrification stress and inflammatory response. Conclusion GFA may protect AP-induced acute liver injury. Its mechanism may be related to its antioxidation, inhibition of nitrification stress, reduction of inflammatory reaction and inhibition of apoptosis.