二氧化硫衍生物引起大鼠血管舒张的细胞信号转导途径

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     

Effect of hydrogen sulfide in comparison to atorvastatin on endothelial damage in cholesterol-fed rabbits

Hydrogen sulfide (H₂S) is an endogenous gaseous molecule, functioning as a physiological regulator. This study aimed to investigate the role of H₂S in atherosclerosis. Rabbits receiving high cholesterol were given atorvastatin (10 mg/kg/day, orally) or sodium sulfide (1.1 mg/kg/day, intramuscular) 2 weeks after commencement of high-cholesterol diet and continued for 4 weeks. Serum lipid profiles, lipid peroxidation indexed as malondialdehyde, glutathione, superoxide dismutase, the vascular adhesion molecule-1, and aortic vascular endothelial growth factor were determined. Rabbits receiving a high-cholesterol diet showed elevated levels of total serum cholesterol, triglycerides, low-density lipoprotein cholesterol, malondialdehyde and vascular adhesion molecule-1, and aortic vascular endothelial growth factor expression and lower levels of high-density lipoprotein cholesterol, glutathione, and superoxide dismutase. Treatment with atorvastatin and sodium sulfide has beneficial effects on serum lipid profile, oxidative damage, vascular adhesion molecule-1, and aortic expression of vascular endothelial growth factor.     

二氧化硫衍生物对大鼠离体主动脉血管环的舒张作用

研究了不同浓度SO2体内衍生物(亚硫酸钠和亚硫酸氢钠混合液)对离体大鼠胸主动脉血管环等长张力的影响一结果表明：①SO2体内衍生物在以去甲肾上腺素(NE)、氯化钾(KCl)颁收缩时对血管均有显著舒张作用，并呈明确的剂量效应关系；②该衍生物在NE预收缩后的舒张作用比KCl预收缩后的作用显著；③左旋硝基精氨酸(L-NNA)、亚甲蓝、普萘洛尔对舒张效应无明显影响；④吲哚美辛可部分地消除该衍生物的舒张效应．总之，SO2体内衍生物具舒张血管作用，此作用不经一氧化氮(NO)介导，而部分地与前列环素(PGI2)有关．图2表1参12。