人参果花青素对对乙酰氨基酚致小鼠肝损伤的保护作用

Protective effect of ginseng fruit anthocyanins against acetaminophen-induced liver damage in mice

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） against acetaminophen（AP） induced liver damage in mice and its possible mechanism. Methods The model of AP induced liver injury was established, and the GFA protection for liver damage was observed. Thirty-two male ICR mice were randomly divided into normal group, AP group, GFA with 200 mg/kg dose group, and GFA with 400 mg/kg group. Colorimetric method was used to assay the contents of serum alanine aminotransferase（ALT） and aspartate aminotransferase（AST）, activity of glutathione（GSH） and malondialdehyde（MDA） content of liver homogenate in mice, and observe liver tissue pathological section. Results GFA obviously reduced the level of ALT in serum, inhibited the level of MDA, and enhanced activity of GSH in liver tissue. The HE and Hoechst 33258 staining results indicated that GFA could obviously improve the degree of liver tissue necrosis and apoptosis, narrow the scope of necrosis, and relieve the inflammatory cell infiltration. By inflammatory factor of i NOS, COX-2 immunohistochemical staining and nitrification stress index of 3-NT immunofluorescence, GFA could inhibit nitration stress and the expression of inflammatory cytokines. Conclusion GFA has certain protective effect on AP-induced acute liver injury and its mechanism may relate to antioxidant effect, inhibition of nitrification stress, alleviation inflammation reaction and inhibiting apoptosis.