【摘要】 探讨二氧化硫(SO2)及其衍生物(Na2SO3/NaHSO3)引起大鼠血管舒张作用与细胞信号转导的关系.采用放射免疫分析技术测定不同浓度SO2衍生物染毒组和正常组大鼠胸主动脉血管环中环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)及前列环素(PGI2)和血栓素(TXA2)的代谢产物6酮前列腺素F1α(6KetoPGF1α)和血栓素B2(TXB2)的浓度,以及腺苷酸环化酶(AC)活性.结果表明:①在离体大鼠胸主动脉血管中,cAMP和6KetoPGF1α的含量随二氧化硫衍生物浓度的增高而显著升高,且呈一定的剂量效应关系;②AC活性也随SO2衍生物浓度的增高而增高;③而cGMP的含量在SO2衍生物各浓度组均略微降低,但只有4mmol/L组降低显著;cAMP/cGMP比值在各浓度组与正常对照组(CK)相比均有显著性升高;④TXB2的含量在各浓度组均无明显变化;但6Keto/TXB2比值显著升高.试验得出,SO2衍生物作用于血管组织产生PGI2,后者通过激活AC使胞内cAMP增高,即通过PGI2—AC—cAMP信号转导途径引起血管舒张,血压下降.表2参13更多还原

【Abstract】 To study cell signal transduction pathway on vasodilatation rats caused by sulfur dioxide derivatives, levels of cAMP, cGMP, 6-Keto-PGF_ 1α, TXB_ 2 and activity of adenylyl cyclase in the isolated aortic rings of rats were determined by radioimmunoassay. The results indicated that SO_ 2 derivatives could greatly increase the levels of cAMP and 6-Keto-PGF_ 1α in the isolated rat aortic rings in a dose-dependent manner; SO_ 2 derivatives also caused large increase in adenylyl cyclase activity in a dose-dependent manner; cGMP level was decreased, cAMP/cGMP ratios were significantly increased at all SO_ 2 groups; no change in TXB_ 2 was observed at all SO_ 2 concentrations tested. However, 6-Keto / TXB_ 2 was significantly increased by exposure to SO_ 2 derivatives at 2 mmol/L and 4 mmol/L. It was demonstrated that SO_ 2 derivatives caused an increase in PGI_ 2, then AC was activated by PGI_ 2 and AC enhanced the production of cAMP, later caused vasodilatation of blood vessel of rats. Tab 2, Ref 13更多还原