cAMP-PKA信号转导在SO2衍生物舒张血管中作用  

Vasodilatation of SO_2 derivatives and cAMP-PKA signal transduction

作　　者：孟紫强[1] 李屹[1] 曹庆玲[1] 

机构地区：[1]山西大学环境科学与工程研究中心,山西大学环境医学与毒理学研究所,太原030006

出　　处：《中国公共卫生》2008年第5期562-564,共3页Chinese Journal of Public Health

基　　金：国家自然科学基金项目(20677035,20477023);山西省自然科学基金项目(20031092)

摘　　要：目的研究环腺苷酸单磷酸-蛋白激酶A(cAMP-PKA)信号转导系统在SO2衍生物舒张血管中的作用。方法当SO2衍生物诱发该血管环舒张时,采用放射免疫法检测血管环组织环腺苷酸单磷酸(cAMP)、环鸟苷酸单磷酸(cGMP)、前列环素(PGI2)和血栓素(TXA2)的稳定代谢产物6-酮-前列腺素F1a(6-keto-PGF1a,6-keto)和血栓素B2(TXB2)的含量,并用32P掺入底物法测定组织中的蛋白激酶A(PKA)活性。结果SO2衍生物可引起血管组织中cAMP、6-kceto(即PGI2)含量及PKA活性增加,其增加程度与内皮无关;SO2衍生物不能引起血管环cGMP和TXB2含量的变化,但可引起cAMP/cGMP和6-keto/TXB2比值显著升高。结论SO2衍生物可使PGI2-cAMP-PKA信号通路活化,这可能是SO2导致血管舒张的机制之一。Objective To study the role of cAMP - PKA signal transduction pathway on vasodilatation ot rat aortic nngs caused by SO2 derivatives. Methods Levels of cAMA, cGMP, 6 - keto - PGF1α, TXB2 in the isolated aortic rings of rats were determined by radioimmunoassay. PKA activity was assayed by transferring phosphorus （32p）into the biotinylated peptide Kemptide, the most specific substrate for PKA. Results Levels of cAMP, 6 - keto （PG12） and PKA activity in isolated aortic rings were increased by SO2 derivatives in a dose - dependent way, which were independent of endothelium; No change of cGMP and TX.B2 in rings with or without endothelium were observed; cAMP/cGMP and 6- keto/TX-B2, ratios were increased significantly. Conclusion The relaxation effect on the rings caused by SO2 derivatives might be mediated partly by the PGI2 - cAMP - PKA signal transduction pathway. SO/SO2, the precursors of SO2 derivatives, might be a new cellular gas signal molecule, more studies are needed to understand its physiological role.

关 键 词：二氧化硫 亚硫酸钠 血管舒张 信号转导 环腺苷酸单磷酸-蛋白激酶A(cANP-PKA) 

分 类 号：R331.32[医药卫生—人体生理学]