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新型气体信号分子硫化氢对低氧性肺动脉高压和肺血管结构重建的调节作用
慢性低氧性肺动脉高压 (HPH) 是临床上许多心肺疾病发生发展过程中伴随或终的病理生理环节,但其发病机制还不清楚.近几年人们已发现一些小气体分子如一氧化氮(NO)、一氧化碳(CO)在调节HPH中具有重要作用[1].近的研究发现,小气体分子H2S也具有与NO和CO相似的作用,但对HPH调节作用的机制不清.本实验通过大鼠低氧模型和其免疫组织化学方法,首次探讨H2S对肺动脉高压与肺血管结构重建的调节作用.
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Chronic alcoholism can damage the cytoskeleton and aggravate neurological deifcits. However, the effect of chronic alcoholism on hippocampal neurons remains unclear. In this study, a model of chronic alcoholism was established in rats that were fed with 6%alcohol for 42 days. Endog-enous hydrogen sulifde content and cystathionine-beta-synthase activity in the hippocampus of rats with chronic alcoholism were signiifcantly increased, while F-actin expression was decreased. Hippocampal neurons in rats with chronic alcoholism appeared to have a fuzzy nuclear mem-brane, mitochondrial edema, and ruptured mitochondrial crista. These findings suggest that chronic alcoholism can cause learning and memory decline in rats, which may be associated with the hydrogen sulfide/cystathionine-beta-synthase system, mitochondrial damage and reduced expression of F-actin.
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硫化氢化学性眼灼伤四例
硫化氢(H2S)引起的化学性眼灼伤俗称"毒气眼病",临床上少见.2007年4月我们收治了4例由H2S引起的化学性眼灼伤患者.
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急性硫化氢中毒后心肌损害的临床观察
某市一石膏矿于1999年5月27日至2006年10月23日发生3起急性硫化氢中毒事故,现分析如下.
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小鼠脑外伤后内源性硫化氢体系的变化
目的:探讨小鼠脑外伤(traumatic brain injury, TBI)后内源性硫化氢(hydrogen sulfide,H2S)体系的变化。方法:利用改良的自由落体装置建立小鼠TBI模型,使用亚甲基蓝法检测血浆及脑组织中内源性H2S浓度。 Western Blot技术观察内源性H2S合成酶胱硫醚-β-合成酶(cystathionine-beta-synthase,CBS)在小鼠TBI后不同时间(1 h、6 h、12 h、1 d、2 d、3 d、7 d)的表达变化。结果:脑组织内源性H2S浓度在小鼠TBI血清、脑皮质及海马组织中变化趋势一致,呈先降低后升高。TBI后大脑皮质和海马组织CBS表达随着外伤时程的延长逐渐降低。结论:内源性H2S在TBI的病理生理过程中起着重要的作用。
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新型气体信号分子硫化氢在心血管疾病中的意义
长期以来,硫化氢(hydrogen sulfide,H2S)被认为是一种无色具有臭鸡蛋气味的有毒气体,大量吸入可导致多种组织器官的损害,严重者可导致死亡.但近年来的研究表明,H2S在心血管系统具有多种生理和病理生理调节作用,被认为是心血管功能调节的新型气体信号分子[1],对其研究是当前生物学领域的崭新课题,具有重要的理论和临床意义.
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AIM: Ischemic post-conditioning ( PC) plays an important role in cardioprotection from ischemia /reperfusion ( I/R) injury in the young heart but not in the aging hearts .The physiological and pathological roles of hydrogen sulfide ( H2 S) in the regulation of cardio-vascular functions have been recognized .Whether H2 S is involved in the recovery of PC-induced cardioprotection in the aging hearts is unclear.METHOD:The male Wistar young rats (3-month-old), the aging rats (24-month-old), primary cultured cardiomyocytes and the aging cardiomyocytes induced by D-galactose suffered from I/R (or H/R) and PC.RESULTS:I/R (or H/R) decreased H2S production rate and cystathionine γ-lyase (CSE) expression, aggravated cardiomyocyte damage , apoptosis, myocardial infarct size and oxidative stress, reduced cardiac function, increased the levels of Bcl-2, cleaved caspase-3 and caspase-9 mRNA and proteins, promo-ted the release of cytochrome c and mPTP opening, down-regulated the phosphorylation of ERK 1/2, PI3K, Akt and GSK-3βand mito-chondrial membrane potential , up-regulated the phosphorylation of IκBα, NF-κB, JNK2 and STAT3, and inhibited PKC-ε transloca-tion and mitochondrial ATP-sensitive K channels (mitoKATP) in isolated young and aging hearts as well as normal and aging cardiomyo-cytes.PC suppressed myocardial I/R injury in the young heart but not in the aging hearts .Supply of NaHS not only increased PC-in-duced cardioprotection in the young hearts and cardiomyocytes , but also attenuated I/R injury and significantly recovered the cardiopro-tective role of PC in the aging hearts and cardiomyocytes .CONCLUSION:The exogenous H 2 S restores PC-induced cardioprotection through inhibiting oxidative stress via the down-regulation of NF-κB and JAK2-STAT3 pathways and mPTP opening by the up-regulation of ERK1/2-GSK-3β, PI3K-Akt-GSK-3βand PKC-ε-mitoKATP pathways in the aging hearts and cardiomyocytes .These findings provide a novel potential target for the treatment of aging ischemic cardiomyopathy .
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硫化氢矿泉水加甘草全身浴治疗银屑病61例体会
我院中医皮肤科10余年来,充分利用硫化氢泉、低渗泉、微温泉,加入适量煮沸半小时后的甘草药液,对银屑病病人进行药浴临床观察,取得了较好疗效.报告如下.1临床资料