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氢气具有选择性抗氧化作用,能控制各种氧化应激相关损伤、炎症反应和细胞坏死。自从2007年后,相关研究论文已经达到500多篇,氢气生物学已经成为一个研究热点。到现在已经有50多种疾病被证明具有潜在的治疗作用,例如常见的糖尿病、动脉硬化、老年性痴呆、巴金森病、尿毒症、肿瘤化疗副作用、脂肪肝。各类器官缺血再灌注损伤、反射性损伤和器官移植后损伤也取得许多动物实验证据。
尽管如此,氢气对人类疾病的治疗作用的确定性证据仍不够全面和充分。到目前只有10多项小规模临床初步研究,证明对中风、巴金森病、尿毒症透析治疗损伤、反射性损伤、类风湿性关节炎症、皮肤疾病、运动后疲劳、代谢综合症等具有一定治疗效果。因此,不仅需要继续开展各类动物实验研究和细胞机制研究,更重要的是应该开展大规模临床实验研究。
上图为细胞凋亡组织化学研究结果,下图为NFkB组织化学染色结果
最近来自多家研究单位,包括解放军总医院、东方肝胆外科医院等七家单位联合开展的一项研究,论文负责作者为东方肝胆外科著名教授杨甲梅。研究结果发现氢气生理盐水注射可以缓解大部分肝脏切除后肝脏功能衰竭,这一研究论文最近在线发表在Clin Res Hepatol Gastroenterol.上。全文:Hydrogen-rich saline attenuates postoperative liver failure after major hepatect.pdf
该研究采用90%肝脏切除大鼠模型,手术后每8小时1次注射氢气饱和生理盐水。结果发现,经过治疗对手术后肝脏功能下降、组织学异常、炎症反应和氧化应激相关改变均有相应缓解作用,该作用可能和NFkB受到抑制有关。
Clin Res Hepatol Gastroenterol. 2014 Feb 3.pii: S2210-7401(13)00265-9. doi:
10.1016/j.clinre.2013.11.007. [Epub aheadof print]
Hydrogen-rich saline attenuatespostoperative liver failure after major hepatectomy in rats.
Tan YC(1), Xie F(2), ZhangHL(3), Zhu YL(4), Chen K(5), Tan HM(5), Hu BS(5), Yang JM(6), Tan JW(7).
A major hepatectomy occasionally lead to acute liverfailure and death. We demonstrated the anti-oxidative and anti-inflammatoryeffects and functional mechanisms of hydrogen-rich saline (HS), a novelantioxidant, on an experimental model of rats after a partial hepatectomy (PH).
The rats underwent a 90% hepatectomy. HS was givenintraperitoneally after the operation and every 8hours after.
HS markedly improved the survival rate of twoexperimental groups after the massive hepatectomy and inhibited increases inserum levels of TBIL, DBIL, ALT and AST. The histopathological analysisdemonstrated that HS attenuated inflammatory changes in the liver. HSadministration markedly lowered the massive hepatectomy induced elevation ofthe serum hyaluronic acid (HA) concentrations. HS inhibited the formation ofone of the markers of oxidative damage, malondialdehyde (MDA), and increasedthe activities of superoxide dismutase (SOD) in liver tissue. In the HS-treatedgroup, increases in inflammatory cytokines, such as TNF-α, IL-6 and HMGB-1,were inhibited in the liver tissue. The NF-κB p65 staining revealed that HSinhibited the activation of the transcription factor nuclear factor kappa B(NF-kB).
HS attenuates the massive hepatectomy induced liverinjury not only by attenuating oxidative damage, but also by reducing theproduction of inflammatory cytokines, such as TNF-α, IL-6 and HMGB-1, in partthrough the inhibition of NF-kB activation.
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