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作 者:井然[1] 钱捷[2] 弓景波[3] 梅竹松[3] 王新兴[3] 钱令嘉[3]
机构地区:[1]南方医科大学第一临床医学院,广东广州510515 [2]福建医科大学公共卫生学院 [3]军事医学科学院基础医学研究所
出 处:《环境与健康杂志》2012年第10期881-883,共3页Journal of Environment and Health
基 金:国家自然科学基金重点项目(30430590)
摘 要:目的观察不同高温环境中热应激大鼠心肌损伤状况,探索血液淋巴细胞中HSP70水平与心肌损伤的相关性规律及其意义。方法50只雄性Wistar大鼠随机分为常温(22~25℃)组,36、37、38、39℃热应激组。以人工高温舱对大鼠进行热暴露。采用电子肛温计检测大鼠肛温,采用八导生理记录仪观测大鼠心电图的变化,采用酶学试剂盒检测大鼠血清乳酸脱氢酶(LDH)和肌酸激酶同工酶(CK—MB)活力,采用Western Blot方法对大鼠外周血淋巴细胞热休克蛋白70(HSP70)含量进行半定量分析。结果与常温组比较,36~39℃组体温均升高(均P〈0.05);37~39℃组Q—T间期延长和R波振幅下降(均P〈0.05);38~39℃组血清中LDH和CK—MB活力升高(均P〈0.05)。淋巴细胞中HSP70表达水平随环境温度的变化呈现不同的变化规律,热环境温度≤37℃时,HSP70表达随气温升高而显著增加(均P〈0.05),热环境温度〉138℃后,HSP70表达随气温升高而下降,但仍显著高于常温组(均P〈0.05)。结论热应激可导致大鼠心肌损伤和外周血淋巴细胞HSP70表达水平发生规律性变化,提示HSP70可能是热应激致心肌损伤的一种生物标志分子,在高温所致心肌损伤发生中具有重要作用。Objective To investigate the myoeardium damage of rats induced by hot environment and its correlation with HSP70 level in blood lymphocytes. Methods Fifty Wistar rats were randomly devided into one normal temperature group and four heat stress groups (36, 37, 38, 39 ℃ ). The artificial chamber with high temperature was used to establish the hot environment for rats. Rectal temperature of rats was detected by electronic thermograph. The electrocardiogram was examined by eight-channel physiological recorder. The activity of LDH and CK-MB were determined with biochemical methods. The expression level of HSP70 in blood lymphocytes was analyzed by Western Blot. Results Compared with normal temperature group,significant increase of rectal temperature in rats was observed in heat stress groups(36, 37, 38, 39 ℃)(P〈0.05). Q-T interval prolongation and R wave amplitude descend were observed in electrocardiogram in heat stress groups(37, 38, 39 ℃ ), and the rate of abnormal electrocardiogram in heat stress groups (36, 37, 38, 39 ℃ ) also increased as the ambient temperature increased (P〈0.05). When environmental temperature was over 38 ℃, the activity of LDH and CK-MB in serum in heat stress groups increased significantly (P〈0.05). In 36 ℃ and 37 ℃ heat stress groups, HSP70 level increased remarkably (P〈0.05) as ambient temperature increased. But when ambient temperature was over 38 ℃, HSP70 expression decreased with increased temperature ,while still significantly higher than the normal temperature group. Conclusion Heat stress may induce the myocardium damage and change of HSP70 expression in blood lymphocytes in rats, which suggests that the HSP70 in blood lymphocytes maybe is a molecular marker and HSP70 plays a role in myocardium injury induced by heat exposure.
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