高温复合脂多糖应激大鼠血浆MDA、SOD的变化规律
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全军“十五”医药卫生科研基金(01MA133);国家重点基础发展计划(973计划)(G200056905).


Changes of plasma malondialdehyde and superoxidase dismutase concentration in LPS-heat co-stressed rats
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    摘要:

    目的:探讨高温与脂多糖(LPS)复合应激大鼠血浆丙二醛(malondialdehyde, MDA)含量、超氧化物歧化酶(superoxide dismutase, SOD)活力等指标的变化规律.方法:雄性SPF级Wistar大鼠随机分为常温生理盐水组(C组)、高温生理盐水组(H组)、常温LPS组(L组)、高温LPS组(HL组),各组下设0、40、80、120 min亚组,每组5只.置动物于模拟气候舱,HL组、H组干球温度(dry bulb temperature, Tdb)为(35.0±0.5)℃,L组、C组Tdb为(26.0±0.5)℃;HL组、L组动物经尾静脉注射LPS 10 mg/kg (浓度为1 mg/ml),H 组、C组动物经尾静脉注射0.9% NaCl 10 ml/kg.检测动物应激0、40、80、120 min时血浆MDA含量、SOD活力的变化.结果:应激120 min时,L组、H组、HL组动物血浆MDA含量、SOD活力均与C组存在显著性差异(P<0.05);HL组动物MDA水平显著升高,SOD活力水平显著下降,与同时相其他各组比较差异有统计学意义(P<0.05).结论:高温与LPS复合应激可能促发、扩大全身炎症反应综合征.

    Abstract:

    Objective.. To investigate the effect of co-exposure to LPS and heat on plasma malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in rats. Methods: Male specific pathogen-free Wistar rats were randomly assigned to the following groups., saline injection+normothermic control (C-Group), saline injection+heat exposure (H-Group), LPS injection+normothermic control (L-Group), and LPS injection+heat exposure (HL-Group). Rats in H-/HL-Group were exposed in a chamber at an ambient dry bulb temperature (Tdb) of (35.0±0. 5)℃ and in C-/L-Group at an ambient Tdb of (26.0+0.5) ℃. Rats in L-/HL-Group were given an intravenous injection of LPS 10 mg/kg via tail veins to induce endotoxemia and in C-/H-Group were given an intravenous injection of 0. 9% NaCl (10 ml/kg) via the tail vein. Mean arterial pressure (MAP) was continually monitored in all rats. Plasma levels of MDA and SOD activity were determined at 0, 40, 80, 120 rain after exposure. Results: There was significant difference in plasma MDA levels and activities of SOD between L-/H-/HL-Group and C-Group (P〈0.05). The rats in HL-Group displayed significantly increased MDA level and decreased SOD activity compared with those in the other 3 groups(P〈0.05). Conelusion. This study suggests that co-exposure to LPS and heat can promote and augment systemic inflammatory response syndrome in rats.

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