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Inhibitive effects of microRNA-34a on protecting against ischemia-reperfusion injury of vital organs in hemorrhagic shock pregnant mice

机译:microRNA-34a对失血性休克妊娠小鼠重要器官缺血再灌注损伤的保护作用

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OBJECTIVE: Hemorrhagic shock is a common vital condition in obstetrics, and major treatment consists of bleeding control and liquid resuscitation. MicroRNA (miR) has been found to regulate multiple diseases. However, its expression profile in hemorrhagic shock or effects on the ischemia-reperfusion injury in pregnant mice has not been reported yet. PATIENTS AND METHODS: This study generated rat hemorrhagic shock pregnant model, on which real-time quantitative PCR was used to measure miR-34a expressions. MiR-34a inhibitor was applied to specifically suppress miR-34a expression. Serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by using the commercial kit. Ischemia-reperfusion injury on rat kidney, lung, liver and intestine tissues was evaluated by using hematoxylin-eosin (HE) staining. RESULTS: In a hemorrhagic shock pregnant rat model, miR-34a expression level was significantly elevated compared to the Normal group (p < 0.05). Application of miR-34a inhibitor effectively suppressed the miR-34a expression in rat kidney, lung, liver and intestine tissues (p < 0.05 compared to normal group). Model rats also had significantly elevated serum MDA and significantly lower SOD levels compared to Normal group (p < 0.05). miR-34a inhibitor reversed this abnorma lity to certain extents (p < 0.05 compared to model group). HE results showed ischemia-reperfusion damage in rat kidney, lung, liver and intestine tissues. miR-34a inhibitor improved such injury. CONCLUSIONS: Suppression of miR-34a could alleviate multi-organ damage after re-perfusion of hemorrhagic shock pregnant rats, probably due to the suppression of oxidative stress. Suppression of miR-34a might work as the treatment target treating multi-organ damage caused by hemorrhagic shock.
机译:目的:失血性休克是产科常见的重要疾病,主要治疗方法包括控制出血和液体复苏。已发现MicroRNA(miR)可以调节多种疾病。然而,尚未报道其在失血性休克中的表达谱或对妊娠小鼠的缺血-再灌注损伤的影响。患者与方法:本研究建立了大鼠失血性休克妊娠模型,在该模型上实时定量PCR用于测量miR-34a的表达。应用MiR-34a抑制剂特异性抑制miR-34a表达。血清丙二醛(MDA)和超氧化物歧化酶(SOD)的水平通过使用商业试剂盒进行测量。使用苏木精-伊红(HE)染色评估大鼠肾脏,肺,肝和肠组织的缺血再灌注损伤。结果:在失血性休克妊娠大鼠模型中,与正常组相比,miR-34a表达水平显着升高(p <0.05)。使用miR-34a抑制剂可有效抑制大鼠肾,肺,肝和肠组织中miR-34a的表达(与正常组相比,p <0.05)。与正常组相比,模型大鼠的血清MDA也显着升高,而SOD水平显着降低(p <0.05)。 miR-34a抑制剂在某种程度上逆转了这种异常(与模型组相比,p <0.05)。 HE结果显示大鼠肾脏,肺,肝和肠组织中缺血-再灌注损伤。 miR-34a抑制剂可改善此类损伤。结论:抑制miR-34a可以减轻失血性休克妊娠大鼠再灌注后的多器官损伤,这可能是由于抑制了氧化应激。抑制miR-34a可能是治疗出血性休克引起的多器官损伤的治疗目标。

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