机构地区:[1]沈阳军区联勤部疾病预防控制中心,辽宁沈阳110034 [2]沈阳工业安装工程南京分公司,江苏南京210029 [3]沈阳药科大学,辽宁沈阳110016
出 处:《工业卫生与职业病》2009年第2期77-80,共4页Industrial Health and Occupational Diseases
摘 要:目的通过对冷应激大鼠脑组织环磷酸腺苷(cAMP)与环磷酸鸟苷(cGMP)含量,腺苷酸环化酶(AC)和磷酸二酯酶(PDE)生物活力的研究,旨在探讨冷应激对中枢神经系统损伤的机制。方法将大鼠分对照组与实验组〔含冷应激组和冷应激恢复组(以下简称恢复组)〕,cAMP、cGMP含量检测采用酶联免疫分析法(ELISA)。AC和PDE的生物活力检测采用放射性同位素法。结果大鼠脑皮质cAMP含量和AC活力:对照组为(0.516±0.271)pmol/mg和(1.67±0.52)pmol/(mg.min),冷应激组为(0.338±0.204)pmol/mg和(1.38±0.15pmol/(mg.min),而恢复组cAMP含量为(0.419±0.197)pmol/mg,与对照组比较,差异有统计学意义(P<0.05)。大鼠脑干cAMP含量和AC活力:对照组为(0.326±0.212)pmol/mg和(2.21±0.13)pmol/(mg.min),冷应激组为(0.297±0.224)pmol/mg和(1.95±0.14)pmol/(mg.min),与对照组比较,差异有统计学意义(P<0.05)。大鼠丘脑下部cAMP含量和AC活力:对照组为(0.651±0.231)pmol/mg和(2.87±0.21)pmol/(mg.min),冷应激组为(0.366±0.219)pmol/mg和(1.36±0.25)pmol/(mg.min);对照组PDE活力为(6.42±0.47)%/(mg.min),而冷应激组为(7.91±0.16)%/(mg.min),与对照组比较,差异有统计学意义(P<0.05)。结论冷应激降低大鼠脑组织不同区域cAMP含量和AC活力,提示,持续冷应激可造成AC-cAMP信号转导通路损伤。Objective Through the study on the effect of cold stress on levels of cAMP(cyclic adenosine mono-phosphate) and cGMP (cyclic guanosine mono-phosphate) and bioactivities of AC (adenylyl eyclase) and PDE(phosphodiesterase)in brain tissues of rat to explore the impairment mechanism of central nerve system induced by cold stress. Methods Wistar rats were divided into the control group, cold stress group and recovery group. The cAMP and cGMP contents were determined by enzyme linked immunosorbent assay. Radioisotope method was used to measure the bioactivities of AC and PDE. Results The content of cAMP and hioactivity of AC in rat cortex of the control group were(0. 516±0. 271)pmol/mg and(1. 67±0.52)pmol/ (mg ·min)respectively, those of the cold stress group were(0. 338±0. 204)pmol/mg and(1.38±0.15)pmol/ (mg·min)respectively. However, the cAMP content in the recovery group was(0. 419±0. 197)pmol/mg. In comparison with the control group the difference was significant, P〈0.05. The content of cAMP and bioactivity of AC in rat brainstem of the control group were(0. 326 ±0. 212) pmol/mg and(2.21±0.13) pmol/ (mg·min)respectively, those of the cold stress group were(0. 297±0. 224)pmol/mg and(1.95±0. 14)pmol/ (mg· min)respectively. In comparison with the control group the difference was significant, P〈0. 05. The content of cAMP and bioactivity of AC in rat hypothalamus of the control group were(0. 651±0. 231)pmol/mg and(2.87±0.21)pmol/(mg · min)respectively; those of the cold stress group were(0. 366±0. 219)pmol/mg and ( 1.36 ± 0. 25 ) pmol/(mg · min) respectively. The PDE activity of the control group was (6.42 ± 0. 47)% / (mg·min), but that of the cold stress group was(7.91 ±0.16)%/(mg· min). In comparison with the control group the difference was significant, P〈0.05. Conclusions The results demonstrate that cold stress could reduce cAMP content and activity of AC in the brain tissues of
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