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作 者:孙辉[1] 高彦辉[1] 郭玲[1] 周令望[1] 刘艺[1] 刘阳[1] 庞博[2] 暴永平 钟学宽[1]
机构地区:[1]哈尔滨医科大学中国疾病预防控制中心地方病控制中心克山病研究所,150081 [2]哈尔滨医科大学04级学生 [3]英国东英格兰大学医学院
出 处:《中国地方病学杂志》2007年第4期372-374,共3页Chinese Jouranl of Endemiology
基 金:黑龙江省教育厅资助项目(10551140)
摘 要:目的 研究Ⅱ相酶和一氧化氮(NO)在低硒病毒性心肌损伤中的变化以及十字花科蔬菜成分菜菔硫烷(SF)的影响。方法 采用低硒和常硒病毒性心肌损伤小鼠模型,观察心肌组织Ⅱ相酶和NO的变化及SF对其的影响。结果 病毒感染使低硒条件下谷胱甘肽硫转移酶(GST)水平增高[(22.46±2.08)×10^3、(19.36±2.03)×10^3U/g,P〈0.05],而常硒条件下使醌还原酶(QR)水平增高[(24.40±1.18)×10^3、(22.04±1.25)×10^3U/g,P〈0.01],各SF保护组Ⅱ相酶活性均明显高于相应未保护组(P〈0.05);病毒感染使小鼠血清NO水平升高(P〈0.01)。常硒SF保护组NO水平显著低于未保护组[(45.98±3.16)、(61.33±8.54)μmol/L,P〈0.01]。结论 SF可通过诱导心肌组织Ⅱ相酶活性.提高抗氧化能力以及降低血清NO水平减轻炎症反应来保护损伤的心肌。Objective To observe the effect of sulforaphane(SF) on coxsackievirus B3m-induced myocardiopathy in Se-deficient mice through phase Ⅱ enzymes activity and nitrogen monoxidum (NO) level. Methods 160 mice were divided into 6 groups, i.e. Se-deficient control group, Se-deficient ± virus group, Se-deficient ± virus ± SF group, Se-adequate control group, Se-adequate ± virus group, Se-adequate ± virus ± SF group. Phase Ⅱ enzymes [glutathione S-transferase (GST) and quinone reductase (QR)] activities of myocardium and serum NO level were examined. Results Virus infection increased myocardial GST activity of Se-deficient mice [ (22.46 ± 2.08) × 10^3 U/g vs (19.36 ± 2.03) × 10^3 U/g, P 〈 0.05] and QR activity of Se-adequate mice[(24.40 ± 1.18) × 10^3 U/g vs (22.04 ± 1.25) × 10^3 U/g, P 〈 0.01 ] ; SF treatment significantly induced activity of myocardial GST and QR of both Se-deficient and Se-adequate viral-infected animal(P 〈 0.05 ). Virus infection increased serum NO level of both Se-deficient and Se-adequate mice (P 〈 0.01 ), and SF treatment significantly decreased serum NO level of Se-adequate viral-infected animals [ (45.98 ± 3.16)μmol/L vs (61.33 ± 8.54)μmol/L, P 〈 0.01 ]. Conclusions SF protect mouse myocardium from damaging by inducing phase Ⅱ enzymes activities and decreasing NO level.
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