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作 者:吕干新[1] 张腾[2] 周娜丹[2] 陈一和[2] 革丽莎[3] 李岳春[2]
机构地区:[1]丽水市中心医院心内科 [2]温州医学院附属第二医院心内科 [3]温州医学院附属第二医院儿科
出 处:《中国临床药理学与治疗学》2013年第12期1332-1337,共6页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:国家自然科学基金(81200165);浙江省自然科学基金(Y2100551)
摘 要:目的:研究卡维地洛对急性柯萨奇B3(CVB3)病毒性心肌炎小鼠的儿茶酚胺及炎症因子IL-6表达水平的影响。方法:随机将80只雄性BALB/C小鼠分为3组:正常对照组(n=20),心肌炎组(n=30),卡维地洛组(n=30)。后两组经腹腔接种CVB3诱发急性病毒性心肌炎,感染24h后卡维地洛组每日灌胃给予卡维地洛10mg/kg,连续14d。于接种第7和14天随机从各组抽取8只小鼠取血后处死并留取心脏等标本。比较干预组与对照组心肌病理改变,采用高效液相色谱-电化学法检测去甲肾上腺素含量,采用RT-PCR法检测心肌IL-6mRNA的表达,采用酶联免疫吸附实验方法检测心肌IL-6蛋白的表达。结果:与心肌炎组比较,卡维地洛组心肌病理损伤明显减轻。与正常组比较,病毒性心肌炎小鼠血浆去甲肾上腺素明显升高,卡维地洛干预后小鼠血浆去甲肾上腺素明显下降(P<0.05)。与正常组比较,心肌炎组心肌IL-6表达明显上调(P<0.05)。与心肌炎组比较,卡维地洛组IL-6表达明显下调(P<0.05)。结论:卡维地洛通过抑制儿茶酚胺对心肌的毒性作用以及下调心肌IL-6表达水平,减轻心肌炎小鼠的心肌损害。AIM: To examine the effects of carvedilol on plasma norepinephrine and myocardial IL-6 production in murine model with the coxsackievirus B3 (CVB3)-induced viral myocarditis. METHODS: Eighty male BALB/C mice were divided into three groups randomly, including normal group, carvedilol group, myocarditis group. The latter two groups were intraperitoneally inoculated with CVB3. Starting 24 h after infection carvedilol was administered orally in a dose of 10 mg · kg-1 d ·-1 for 14 days continuously. Myocarditis group and normal group were used with same dose PBS. Eight mice who were randomly taken from each groups were kill- ed on day 7 or 14. Myocardial histopathology changes, the heart weight/body weight ratio, the plasma norepinephrine, the mRNA and protein expression of myocardial IL-6 were studied. RESULTS: Carvedilol significantly attenuated myocardial lesions and decreased the heart weight/body weight ratio(P〈0.05). The plasma norepinephrine was decreased, the mRNA and protein expression of IL-6 was down regulated remarkably in the carvedilol group compared with the myocarditis group (P 〈 0.05). CONCLUSION: Carvedilol protects against CVB3-induced viral myocarditis in mice. Carvedilol exerts some of its beneficial effects by decreasing the plasma catecholamine levels and down-regulating the expression of IL-6.
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