Department of Emergency, Fengxiang County Hospital, Baoji, China.
Eur Rev Med Pharmacol Sci. 2018 Mar;22(6):1812-1818. doi: 10.26355/eurrev_201803_14600.
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.
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.
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.
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.
失血性休克是产科常见的危急情况,主要治疗方法包括控制出血和液体复苏。MicroRNA(miR)已被发现可调节多种疾病。然而,其在失血性休克中的表达谱或对妊娠小鼠缺血再灌注损伤的影响尚未报道。
本研究建立了大鼠失血性休克妊娠模型,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 的表达。采用商业试剂盒测定血清丙二醛(MDA)和超氧化物歧化酶(SOD)水平。通过苏木精-伊红(HE)染色评估大鼠肾、肺、肝和肠组织的缺血再灌注损伤。
在失血性休克妊娠大鼠模型中,与正常组相比,miR-34a 的表达水平显著升高(p < 0.05)。miR-34a 抑制剂的应用有效抑制了大鼠肾、肺、肝和肠组织中 miR-34a 的表达(与正常组相比,p < 0.05)。模型大鼠的血清 MDA 水平显著升高,SOD 水平显著降低,与正常组相比(p < 0.05)。miR-34a 抑制剂在一定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、肺、肝和肠组织发生缺血再灌注损伤。miR-34a 抑制剂改善了这种损伤。
抑制 miR-34a 可减轻失血性休克再灌注后大鼠多器官损伤,可能是通过抑制氧化应激。抑制 miR-34a 可能成为治疗失血性休克引起的多器官损伤的治疗靶点。