Role of mitochondrial autophagy mediated by PINK1/Parkin signaling pathway in severe pneumonia
Objective To investigate the role of mitochondrial autophagy mediated by PINK1(homologous phosphatase tensin induced kinase 1)/Parkin(Parkinson's protein)signaling pathway in severe pneumonia of rats.Methods Twenty rats were randomly divided into control group and model group(severe pneumonia model),with 10 rats in each group,to explore the effects of severe pneumonia on lung function and pathology in rats.Then,30 rats were randomly divided into control group,model group and mdivi-1(mitochondrial autophagy inhibitor)group,with 10 rats in each group,to further explore the effects of severe pneumonia on mitochondrial autophagy indicators of rats.Results Compared with the control group,the resting ventilation volume[(3.44±0.22)vs.(1.58±0.18)mL/min]and airway resistance ratio(77.48±3.84 vs.47.76±5.54)in the model group were decreased(P＜0.05).In the model group,the lung tissue was injured and a large number of inflammatory cells were infiltrated.The protein and mRNA expression levels of Parkin,PINK1 and microtubule-associated protein1 light chain 3 in lung tissues of model group were increased(P＜0.05).Compared with model group,the ratio of resting ventilator-to-airway resistance in mdivi-1 group increased(P＜0.05).The injury and inflammatory infiltration of lung tissue were improved in mdivi-1 group.The expression levels of Parkin,PINK1 and microtubule-associated protein1 light chain 3 protein and mRNA in lung tissues of mdivi-1 group were decreased(P＜0.05).Conclusion Mdivi-1 can improve the abnormal lung function structure in rats with severe pneumonia,and the mechanism may be related to mitochondrial autophagy mediated by PINK1/Parkin signaling pathway.
Severe pneumoniamitochondrial autophagyhomologous phosphatase tensin induced kinase 1Parkinson's proteinsignaling pathway
NETL
NSTL
万方数据
