论文部分内容阅读
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: To investigate the effects of cAMP and cGMP, AC and phosphodiesterase (PDE) on the brain tissue of rats with cold stress To explore the mechanism of cold stress on the central nervous system damage. Methods The rats were divided into control group and experimental group (including cold stress group and cold stress recovery group (hereinafter referred to as the recovery group)], cAMP, cGMP content was detected by enzyme-linked immunosorbent assay (ELISA). The bioactivities of AC and PDE were measured by radioisotope method. Results The levels of cAMP and AC in cerebral cortex were (0.516 ± 0.271) pmol / mg and (1.67 ± 0.52) pmol / (mg.min) in control group and (0.338 ± 0.204) pmol / mg and (1.38 ± 0.15pmol / (mg.min), while the recovery group cAMP content was (0.419 ± 0.197) pmol / mg, compared with the control group, the difference was statistically significant (P < AC was (0.326 ± 0.212) pmol / mg and (2.21 ± 0.13) pmol / (mg.min) in the control group and (0.297 ± 0.224) pmol / mg and (1.95 ± 0.14) pmol / (0.651 ± 0.231) pmol / mg and (2.87 ± 0.21) pmol / mg, respectively, compared with the control group, the difference was statistically significant (P <0.05) (0.366 ± 0.219) pmol / mg and (1.36 ± 0.25) pmol / (mg.min) respectively in the cold stress group and (6.42 ± 0.47)% / (mg.min) in the control group , While it was (7.91 ± 0.16)% / (mg.min) in cold stress group, which was significantly different from that in control group (P <0.05) .Conclusion Cold stress reduces cAMP content in different regions of rat brain and AC activity, suggesting that continuous cold stress can cause AC-cAMP signal transduction pathway damage.