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.
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 rathemorrhagic 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.