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目的:探讨硫化氢(hydrogen sulfide,H2S)对过氧化氢(hydrogen peroxide,H2O2)引起的大鼠离体胸主动脉损伤的保护作用和机制。方法:分离正常大鼠胸主动脉,制备主动脉环,利用300μmol/L H2O2建立大鼠胸主动脉环氧化应激损伤模型。25、50、100μmol/L的硫氢化钠(sodium hydrosulfide,NaHS)预处理后再用H2O2损伤大鼠胸主动脉环,应用血管功能检测张力仪比较各组舒张功能,并采用二氢乙啶(dihydroethidium,DHE)荧光染色法测定活性氧自由基(reactive oxygen species,ROS)的生成。Western blot法检测大鼠胸主动脉环中ERK1/2和磷酸化ERK1/2(p-ERK1/2)蛋白的表达。结果:300μmol/L的H2O2可引起大鼠胸主动脉环内皮依赖性舒张功能受损,50、100μmol/L的NaHS预处理后该损伤得到明显改善,使H2O2诱发的ROS亦显著减少。同时,H2O2可激活大鼠胸主动脉组织中的MAPK/ERK通路,使其磷酸化水平增加,而给予50、100μmol/L的NaHS预处理后可抑制该作用。结论:硫化氢对H2O2致大鼠胸主动脉氧化应激性损伤有保护作用,其机制可能与调节ERK信号通路有关。
Objective: To investigate the protective effect and mechanism of hydrogen sulfide (H2S) on rat thoracic aorta injury induced by hydrogen peroxide (H2O2). Methods: Thoracic aorta was isolated from the normal rat thoracic aorta and the aortic rings were prepared. The epicardial oxidative stress injury model of thoracic aorta was established by 300 μmol / L H2O2. 25, 50 and 100μmol / L sodium hydrosulfide (NaHS) were pretreated with H2O2, then the thoracic aorta rings were injured by H2O2. The diastolic function of each group was compared with vascular function test tension meter, dihydroethidium (DHE) was used to determine the production of reactive oxygen species (ROS). Western blot was used to detect the expression of ERK1 / 2 and phosphorylated ERK1 / 2 (p-ERK1 / 2) in the thoracic aorta. RESULTS: 300μmol / L H2O2 could induce endothelium-dependent vasodilation in rat thoracic aorta. The injury was markedly improved after 50,100μmol / L NaHS pretreatment, and the H2O2-induced ROS was also significantly reduced. At the same time, H2O2 could activate the MAPK / ERK pathway in the thoracic aorta and increase its phosphorylation. However, pretreatment with 50 and 100μmol / L NaHS inhibited this effect. CONCLUSION: Hydrogen sulfide has a protective effect on oxidative stress-induced injury of thoracic aorta induced by H2O2, which may be related to the regulation of ERK signaling pathway.