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Effects of Simulated Heat Waves with Strong Sudden Cooling Weather on ApoE Knockout Mice

机译:强骤冷天气模拟热浪对ApoE基因敲除小鼠的影响

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This study analyzes the mechanism of influence of heat waves with strong sudden cooling on cardiovascular diseases (CVD) in ApoE?/? mice. The process of heat waves with strong sudden cooling was simulated with a TEM1880 meteorological-environment simulation chamber according to the data obtained at 5 a.m. of 19 June 2006 to 11 p.m. of 22 June 2006. Forty-eight ApoE?/? mice were divided into six blocks based on their weight. Two mice from each block were randomly assigned to control, heat wave, temperature drop, and rewarming temperature groups. The experimental groups were transferred into the climate simulator chamber for exposure to the simulated heat wave process with strong sudden temperature drop. After 55, 59, and 75 h of exposure, the experimental groups were successively removed from the chamber to monitor physiological indicators. Blood samples were collected by decollation, and the hearts were harvested in all groups. The levels of heat stress factors (HSP60, SOD, TNF, sICAM-1, HIF-1α), cold stress factors (NE, EPI), vasoconstrictor factors (ANGII, ET-1, NO), and four items of blood lipid (TC, TG, HDL-C, and LDL-C) were measured in each ApoE?/? mouse. Results showed that the heat waves increased the levels of heat stress factors except SOD decreased, and decreased the levels of vasoconstrictor factors and blood lipid factors except TC increased. The strong sudden temperature drop in the heat wave process increased the levels of cold stress factors, vasoconstrictor factors and four blood lipid items (except the level of HDL-C which decreased) and decreased the levels of heat stress factors (except the level of SOD which increased). The analysis showed that heat waves could enhance atherosclerosis of ApoE?/? mice. The strong sudden temperature drop during the heat wave process increased the plasma concentrations of NE and ANGII, which indicates SNS activation, and resulted in increased blood pressure. NE and ANGII are vasoconstrictors involved in systemic vasoconstriction especially in the superficial areas of the body and conducive to increased blood pressure. The increase in the blood lipid levels of TG, LDL-C, TC, and LDL-C/HDL-C further aggravated CVD. This paper explored the influence mechanism of the heat waves with sudden cooling on CVD in ApoE?/? mice.
机译:本研究分析了突然骤冷的热波对ApoE2中心血管疾病(CVD)的影响机理。老鼠。根据2006年6月19日凌晨5点至晚上11点获得的数据,使用TEM1880气象环境模拟室对强烈骤冷的热波过程进行了模拟。于2006年6月22日发布。48个ApoE?根据小鼠的体重将其分为六个块。将来自每个块的两只小鼠随机分配为对照组,热波组,温度下降组和温热组。实验组被转移到气候模拟室中,以暴露于具有剧烈突然温度下降的模拟热波过程中。暴露55、59和75小时后,将实验组依次从试验箱中取出以监测生理指标。抽血收集血样,并在所有组中收集心脏。热应激因子(HSP60,SOD,TNF,sICAM-1,HIF-1α),冷应激因子(NE,EPI),血管收缩因子(ANGII,ET-1,NO)和四类血脂( TC,TG,HDL-C和LDL-C)在每个ApoE /?中测量。老鼠。结果表明,热浪增加了热应激因子的水平,而SOD降低了;热收缩因子和血脂因子的水平降低了,而TC增加了。在热波过程中强烈的突然温度下降增加了冷应激因子,血管收缩因子和四种血脂水平(HDL-C水平下降除外),而热应激因子水平(SOD水平除外)增加)。分析表明,热浪可以增强ApoEβ/α的动脉粥样硬化。老鼠。在热波过程中强烈的突然温度下降增加了NE和ANGII的血浆浓度,这表明SNS活化,并导致血压升高。 NE和ANGII是参与全身血管收缩的血管收缩剂,尤其是在人体浅表区域,有助于血压升高。 TG,LDL-C,TC和LDL-C / HDL-C的血脂水平升高进一步加重了CVD。本文探讨了突然冷却的热波对ApoE /?中CVD的影响机理。老鼠。

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