【摘 要】
：
Objective Hydrogen (H2) attenuates the development of atherosclerosis in mouse models.We aimed to examine the effects of H2 on atherosclerotic plaque stability.Methods Low-density lipoprotein receptor
【机 构】
：
Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis,TaiSh
【出 处】
：
第二届氢分子生物医学学术交流会暨中国医疗保健国际交流促进会氢分子生物医学专业委员会第二次会议
论文部分内容阅读
Objective Hydrogen (H2) attenuates the development of atherosclerosis in mouse models.We aimed to examine the effects of H2 on atherosclerotic plaque stability.Methods Low-density lipoprotein receptor knockout (LDLR-/-) mice fed an atherogenic-diet were dosed daily with H2 and/or simvastatin.In vitro studies were carried out in oxidized-LDL (ox-LDL)-stimulated macrophage-derived foam cell model treated with or without H2.Key Results H2 or simvastatin significantly enhanced plaque stability by increasing levels of collagen and smooth muscle cells, as well as reducing macrophage and lipid levels in plaques.The decreased numbers of dendritic cells and increased numbers of regulatory T cells in plaques further supported the stabilizing effect of H2 or simvastatin.Moreover, H2 treatment decreased serum ox-LDL level and apoptosis in plaques with concomitant inhibition of endoplasmic reticulum stress (ERS) and reduction of ROS accumulation in the aorta.In vitro, like ERS inhibitor 4-phenylbutyric acid, H2 inhibited ox-LDL-or tunicamycin (an ERS inducer)-induced ERS response and cell apoptosis.In addition, like ROS scavenger N-acetyl-cysteine, H2 inhibited ox-LDL-or Cu2+ (an ROS inducer)-induced reduction in cell viability and increase in cellular ROS.Also, H2 increased Nrf2 (NF-E2-related factor-2, an important factor in antioxidant signaling) expression and Nrf2 inhibitor abolished the protective effect of H2 on ox-LDL-induced cellular ROS production.Conclusions The inhibitory effects of H2 on the apoptosis of macrophage-derived foam cells, which take effect by suppressing the activation of ERS pathway and by activating Nrf2 antioxidant pathway, might lead to an improvement in atherosclerotic plaque stability.
其他文献
氢气作为一种功能性气体已经用于各类慢性疾病的预防和保健，但是氢气在体内脏器的代谢和分布却没有得到揭示，本文通过放射药学的方法，观察吸入氢气后各个脏器内氢气的代谢量，从而为临床和科研提供详实的数据.目的：观察吸入氚气(H3气)以后各类组织内氚元素的含量.方法：电解氚气水，得到氚气，将小鼠放置在密闭的空间内，给予氚气空气混合气，三天后解剖，并分析组织内氚的含量.结果：Samples from Mice
斑块的解剖类型稳定斑块 不稳定斑块 破裂斑块易损斑块的破裂是临床事件的诱发因素影响斑块稳定性的因素及其机制斑块内细胞凋亡H2 increases atherosclerotic plaque stability in LDLR-/-mice H2 reduces ox-LDL-induced intracellular lipid accumulation in RAW264.7 cells H2
概要 本研究主要探究富氢生理盐水对大鼠腹部皮瓣缺血再灌注损伤引起的细胞凋亡的保护性作用目的：探究富氢生理盐水对大鼠腹部皮瓣缺血再灌注损伤引起的细胞凋亡的保护性作用。
目录·肠道氢气和长寿的关系·年轻人和老人肠道产氢比较·氢气可以消耗TMA,抗动脉粥样硬化日本百岁老人氢呼气浓度增加Original Article
[目的]明确氢饱和生理盐水(HRS)是否具有大鼠LIRD的保护作用,进一步明确HRS是否通过调控SirT1分子发挥抗LIRD的作用.[方法]大鼠经10000± 100 lux光照3h后,采用视觉电生理ERG和H.E染色法检测大鼠光损伤视网膜程度,采用Western Blotting或(和)实时定量PCR检测SirT1、caspase-3、Bcl-2、Bax蛋白或(和)mRNA表达情况.同时,应用S
目的：探究磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)信号通路在氢气保护小鼠心肌缺血再灌注损伤时的作用.方法：健康雄性C57 BL/6小鼠随机分为8组(n=20)：假手术组(Sham组)、心肌缺血再灌注组(I/R组)、氢气治疗组(I/R+H2组)、氢气+LY294002组(I/R+H2+LY组)、氢气+Wortmannin组(I/R+H2+W组)、LY294002组(I/R+LY组)、Wor
一、疾病产生的根本原因人为什么会生病基因心理外露层冰山层基础层原因层stress各种刺激(应激原神经内分泌反应非特异性全身反应提高对刺激的防御适应能力以交感-肾上腺髓质和下丘脑-垂体-肾上腺皮质反应为主细胞应激(cell stress)是细胞对环境因素导致大分子损伤的一种防御反应,目的是对抗伤害、修复损伤、增加对损伤的耐受性,以最终保护细胞和/或通过细胞死亡过程最终除去损伤后不能修复的细胞.
[目的]明确氢饱和生理盐水(HRS)是否具有大鼠LIRD的保护作用，进一步明确HRS是否通过调控SirT1分子发挥抗LIRD的作用.[方法]大鼠经10000± 100 lux光照3h后，采用视觉电生理ERG和H.E染色法检测大鼠光损伤视网膜程度，采用Western Blotting或(和)实时定量PCR检测SirT1、 caspase-3、Bcl-2、 Bax蛋白或(和)mRNA表达情况.同时，应
我们所了解的氢气●化学上具有还原性●生理学上属于惰性气体氢氧潜水●潜水时呼吸高压气体●氢气和氧气混合气●大深度长时间潜水潜水医学所了解的氢气●分子量很小,扩散速度快,呼吸阻力小●氢氧潜水至今发展有近百年历史●呼吸浓度99.7％氢气,700米水深,工作1 4天氢气的安全性氢气的安全性●超大剂量人体试验安全●大肠可以产生氢气●欧盟美国官方文件安全无毒,效果突出
Objective: The aim of this study was to investigate the effects of hydrogen-rich saline on osteoarthritis in rabbit model.Materials and Methods: Fifty rabbits were randomly divided into five groups: c