摘要
目的构建离体血管H2O2氧化损伤模型,并初步探讨其损伤机制,实验超氧化物歧化酶(superoxide dismutase,SOD)对该损伤的修复作用。方法采用大鼠离体胸主动脉环,构建H2O2氧化损伤血管模型,通过乙酰胆碱(acetylcho-line,ACh)引起的舒张评价该模型的内皮功能;通过硝普钠(nitroprusside sodium,SNP)引起的舒张及苯肾上腺素(phenylephrine,PE)引起的收缩评价该模型的平滑肌功能。同时,用120U·ml-1的SOD作用于该模型30min,评价SOD对模型损伤的修复作用。结果H2O2氧化损伤的血管,对SNP引起的舒张及PE引起的收缩无影响,而对ACh引起的内皮依赖性舒张程度降低,120U·ml-1 SOD作用后,能明显改善该模型的氧化损伤状态。结论H2O2 1mmol·L-110min能够氧化损伤大鼠胸主动脉内皮,120U·ml-1的SOD可以较好地修复H2O2造成的内皮损伤。
Aim To establish the vascular endothelial damage model by H2O2 treatment and explore the underlying mechanism and demonstrate the therapeutic effect of SOD on endothelial dysfunction induced by H2O2 oxidation. Methods H2O2 was used to induce endothelium damage in the rat aortic ring. Endothelial function was examined by acetylcholine（ACh） induced relaxation. Smooth muscle function was evaluated by nitroprusside sodium （ SNP ） derived vasodilation and phenylephrine （PE） produced contraction. SOD （ 120 U ·ml^-1） was incubated for 30 minutes with the H2O2 -damaged endothelium to test the repairing effect of SOD. Results The SNP derived vasodilation and PE produced eontraction were not affected by H2O2 treatment. However, the vasodilation by ACh had been significantly attenuated in H2O2 induced endothelium damage model. SOD significantly restored the relaxant effect of ACh. Conclusion H2O2 treatment can damage the rat blood vessel endothelium and SOD can recover oxidative induced endothelium damage.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2009年第7期884-887,共4页
Chinese Pharmacological Bulletin
基金
国家科技部"十一五"支撑计划资助项目(No2006BAIⅡB08-03)
上海市教委高校一氧化氮与炎症医学E研究院计划资助项目(NoE-04010)
上海市科委国际技术转移专项(No08430711300)
上海市科委中药现代化专项(No08DZ1972104)
上海中医药大学科研资助项目
