汉防己多糖对急性酒精性肝损伤小鼠氧化应激及肝细胞凋亡的影响
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篇名: 汉防己多糖对急性酒精性肝损伤小鼠氧化应激及肝细胞凋亡的影响
TITLE:
摘要: 目的:探讨汉防己多糖对急性酒精性肝损伤小鼠的保护作用及其机制。方法:将60只小鼠随机分为空白对照组(生理盐水)、模型组(生理盐水)、联苯双酯组(阳性对照,150 mg/kg)和汉防己多糖低、中、高剂量组(100、200、400 mg/kg),每组10只,ig给药,每天1次,连续7 d。末次给药1 h后,除空白对照组外其余各组小鼠均ig 50%乙醇(0.1 mL/10 g)溶液复制急性酒精性肝损伤模型。12 h后,测定小鼠血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平以及肝组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)水平;苏木精-伊红染色观察小鼠肝组织病理改变;流式细胞术检测肝细胞凋亡率。结果:与空白对照组比较,模型组小鼠肝组织发生水肿、细胞排列紊乱及局部坏死等病变,血清中ALT、AST水平和肝组织中MDA水平以及肝细胞凋亡率显著升高,肝组织中SOD、GSH、GSH-Px水平显著降低,差异均有统计学意义(P<0.01)。与模型组比较,汉防己多糖中、高剂量组小鼠肝组织细胞变性和坏死程度均减轻;除汉防己多糖低剂量组小鼠肝细胞凋亡率降低不明显外,其余各给药组小鼠上述指标均显著改善(P<0.05或P<0.01)。结论:汉防己多糖对急性酒精性肝损伤小鼠具有明显的保护作用,其机制可能与抗氧化应激及减少肝细胞凋亡有关。
ABSTRACT: OBJECTIVE: To explore the protective effect and its mechanisms of Sinomenium acutum polysaccharide on mice with acute alcoholic liver injury. METHODS: 60 mice were randomly divided into blank control group (normal saline), model group (normal saline), bifendate group (positive control, 150 mg/kg) and S. acutum polysaccharide low-dose, medium-dose, high-dose groups (100, 200, 400 mg/kg), 10 in each group, intragastrically administrated, once a day, for continual 7 d. 1 h after last administration, mice received 50% ethanol (0.1 mL/10 g) intragastrically to induce acute alcoholic liver injury model except for those in blank control group. After 12 h, alanine aminotransferase (ALT), aspartate aminotransferase (AST) levels in serum, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px) levels in liver tissue of mice were determined; hematoxylin-eosin staining was conducted to observe the pathological changes in liver tissue; flow cytometry was used to detect the cell apoptosis rate. RESULTS: Compared with blank control group, mice in model group showed pathological changes in edema, disordered cell arrangement and local necrosis; ALT and AST levels in serum, MDA level in liver tissue and hepatocyte apoptotic rate were significantly increased, while the SOD, GSH and GSH-Px levels in liver tissue were significantly decreased, with statistical significances (P<0.01). Compared with model group, cell degeneration and necrosis degree of mice were improved in S. acutum polysaccharide medium-dose and high-dose groups; except for cell apoptosis rate of liver in S. acutum polysaccharide low-dose group was not decreased significantly, the above-mentioned indicators in other treatment groups were significantly improved (P<0.05 or P<0.01). CONCLUSIONS: S. acutum polysaccharide shows obvious protective effect on mice with acute alcoholic liver injury, its mechanism might relate to anti-oxidation stress and inhibiting hepatocyte apoptosis.
期刊: 2017年第28卷第7期
作者: 徐博,沈楠,安英,李妍,李贺,赵南晰,吴畏难
AUTHORS: XU Bo,SHEN Nan,AN Ying,LI Yan,LI He,ZHAO Nanxi,WU Weinan
关键字: 汉防己多糖;急性酒精性肝损伤;抗氧化;细胞凋亡;小鼠
KEYWORDS: Sinomenium acutum polysaccharide; Acute alcoholic liver injury; Anti-oxidation; Cell apoptosis; Mice
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