首页> 美国卫生研究院文献>International Journal of Clinical and Experimental Pathology >Protective effects of hydrogen-rich saline against renal ischemia-reperfusion injury by increased expression of heme oxygenase-1 in aged rats
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Protective effects of hydrogen-rich saline against renal ischemia-reperfusion injury by increased expression of heme oxygenase-1 in aged rats

机译:血红素加氧酶-1表达增加对富氢生理盐水对肾脏缺血再灌注损伤的保护作用

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摘要

Objective: Oxygen free radicals (ROS) are considered to be one of the important factors involved in the pathophysiology of aged renal ischemia-reperfusion (I/R) injury. Hydrogen gas has been reported to alleviate I/R injury by scavenging free radicals. The aim of this study was to evaluate the effect of hydrogen-rich saline (HRS) on renal I/R injury in aged rats. Materials and methods: A rat model of renal I/R injury was induced by 45-min occlusion of the bilateral renal pedicles and 24-h reperfusion. Physiological saline or HRS (8 ml/kg) was administered intraperitoneally 5 min before reperfusion. Parameters indicating renal function (blood urea nitrogen (BUN) and serum creatinine (SCr)) and those indicating oxidative stress (tissue levels of malondialdehyde (MDA) and 8-hydroxy-deoxyguanosine (8-OHdG), tissue activities of superoxide dismutase (SOD), and tissue expression of heme oxygenase-1 (HO-1)) were measured. Results: After I/R injury, BUN, SCr, tissue levels of MDA and 8-OHdG, and gene expression of HO-1 were all significantly increased while tissue activities of SOD were significantly decreased. HRS reversed these changes, with the exception of HO-1 expression, which was increased further, and improved renal morphology. Conclusions: HRS improves the renal response to I/R in aged rats, possibly by reducing oxidative stress and upregulating HO-1 gene expression.
机译:目的:氧自由基(ROS)被认为是老年肾脏缺血再灌注(I / R)损伤的病理生理学的重要因素之一。据报道,氢气通过清除自由基来减轻I / R损伤。这项研究的目的是评估富氢盐水(HRS)对老年大鼠肾脏I / R损伤的影响。材料与方法:闭塞双侧肾蒂45分钟并再灌注24小时,以致大鼠肾I / R损伤。再灌注前5分钟腹腔注射生理盐水或HRS(8 ml / kg)。指示肾功能的参数(血尿素氮(BUN)和血清肌酐(SCr))以及指示氧化应激的参数(丙二醛(MDA)和8-羟基-脱氧鸟苷(8-OHdG)的组织水平,超氧化物歧化酶(SOD)的组织活性),并测量血红素加氧酶-1(HO-1))的组织表达。结果:I / R损伤后,BUN,SCr,MDA和8-OHdG的组织水平以及HO-1的基因表达均显着增加,而SOD的组织活性则显着降低。 HRS逆转了这些变化,HO-1表达除外,HO-1表达进一步增加并改善了肾脏的形态。结论:HRS可能通过降低氧化应激和上调HO-1基因表达来改善老年大鼠的肾脏对I / R的反应。

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