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机构地区:[1]北华大学医学院生化教研室,吉林132001 [2]吉林铁路疾病预防控制所 [3]吉林大学中日联谊医院
出 处:《中国地方病防治》2008年第1期18-20,共3页Chinese Journal of Control of Endemic Diseases
基 金:吉林省科技厅资助课题(200302-05)
摘 要:目的在大鼠心肌线粒体(Mt)自由基损伤的体外实验中,观察山葡萄多酚(PVAR)的保护作用,为预防和治疗克山病提供实验依据。方法利用Fe2+/维生素C(vitamin C,VitC)系统产生.OH,体外对Wistar大鼠心肌Mt诱导损伤。实验分为正常对照组、诱导损伤组和预先加PVAR再诱导损伤组,观察各组Mt细胞色素C氧化酶、SOD活性,膜磷脂和MDA含量。结果.OH引起Mt显著损伤。与损伤组比较,PVAR(终浓度25、50、100mg/L)可使受损Mt的膜磷脂降解抑制(P<0.05),MDA形成明显减少(P<0.01),细胞色素C氧化酶和SOD活性增高(P<0.05)。高剂量PVAR组与对照组比较无显著差异。结论PVAR对氧应激造成的心肌Mt损伤具有保护作用,保护机制是直接减少氧自由基的生成。Objective To study the protective effects of the polyphenols of vitis amurensis Rupr(PVAR) on rat heart mitochondria injury induced by oxygen stress, Metheds In vitro experiment of rat heart mitochondria, vitamin C and FeSO4 played as an injury agent, PVAR played as a protective agent. Experiments were designed into 3 groups: blank group, injury group and PVAR + injury group. The mitochondrion Cytochrome C oxidase and SOD activity were examined. The mitochondrion membrane phospholipid and MDA were determined. Results ·OH resulted in severe mitochondria injuries and the injuries was alleviated by PVAR( content of 25, 50, 100mg/L). The decomposability of the injured mitochondria phospholipid was decreased( P 〈 0.05), the lipid peroxidation was decreased( P 〈0.01), the Cytochrome C oxidase and SOD activities was increased( P 〈0.05). Conclusion PVAR protected the injury rat heart mitochondria by antagonizing the free radical.
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