MiR-148a Attenuates Hepatic Ischemia/Reperfusion Injury In Mice Via Targeting CaMKⅡα

Objective:To evaluate the impact of mi R-148 a on hepatic I/R via inhibiting Ca MKIIα.Method:Liver I/R model in mice was built. Expression of Ca MKIIα was detected by Western Blot. m RNA level of mi R-148 a, Ca MKIIα, TNF-α and IL-1β were analyzed by q RT-PCR. HE staining was conducted to observe morphological changes of each group. TUNEL was performed to evaluated degree of hepatocellular apoptosis in each group. Results : q RT-PCR data showed that mi R-148 a was elevated, while Ca MKIIα was downregulated. The result of Pearson linear regular analysis suggested that they were negative correlation after hepatic I/R(r=-0.9656, p<0.001). While therapy by exogenous mi R-148 a, protein expression of Ca MKIIα detected by Western Blot(mi R-148 a mimics vs mi R-148 a control,p=0.008), m RNA level of TNF-α(mi R-148 a mimics vs mi R-148 a control,p=0.006)and IL-1β(mi R-148 a mimics vs mi R-148 a control,p=0.005)analyzed by q RT-PCR, level of inflammatory cells infiltration and liver cells necrosis determined by HE staining(mi R-148 a mimics vs mi R-148 a control,p=0.03), level of hepatocellular apoptosis evaluated by TUNEL(mi R-148 a mimics vs mi R-148 a control,p=0.005)were all downregulation.Conclusion:mi R-148 a may alleviate hepatic I/R injury in mouse by compressing Ca MKIIα. In this study, we simply explore the possible mechanism of mi R-148 a attenuating inflammation and hepatic dysfunction induced by hepatic I/R injury. Our results provide clinical targeted treatment for hepatic I/R injury a solid experimental foundation and theoretical basis, which has certain clinical application prospect.