Annexin-A1 tripeptide alleviates lung ischemia-reperfusion injury by promoting lung autophagy in rats

Abstract

Abstract Research on the mechanism and protective measures of lung injury caused by CPB has attracted extensive attention. But the exact mechanism is still being explored. This study explored the role of autophagy in CPB lung injury by establishing the left lung ischemia-reperfusion injury model of rats and observing the relationship between CPB lung injury and autophagy. The effects of exogenous membrane tripeptide (AnxA1sp) on lung injury and autophagy in rats were investigated. Compared with the control group, the expressions of autophagy bodies and autophagy-related proteins in the lung tissue of rats after CPB were increased in the model group. With the aggravation of lung injury, autophagy was significantly increased and the degradation of autophagy was blocked. Autophagy was involved in the occurrence and development of CPB lung injury. In the rat model group of AnxA1-/-, lack of AnxA1 can cause insufficient autophagy and aggravated lung injury in CPB rats. The addition of exogenous AnxA1sp can reduce lung I/R injury in CPB rats, activate lung autophagy, promote autophagy flow, reduce the release of lung inflammatory factors, reduce lung pathological injury, and improve lung function. In conclusion, regulating the autophagy of lung tissue can produce a lung protection effect.