Respirable fine particulate matter (PM2.5) aggravates cerebral ischemia-reperfusion injury in rats by inducing high expression of LOX-1/ NF-κB

Abstract

Abstract Objective:To investigate the mechanism of exacerbating cerebral ischaemia/reperfusion injury in rats after PM2.5 exposure. Methods: Eight-week-old SD male rats were selected and randomly grouped into the following groups: control group, I/R group, I/R+PM2.5 low concentration group, I/R+PM2.5 medium concentration group, I/R+PM2.5 high concentration group, and the rats were given the appropriate interventions.The volume of cerebral infarction, the scores of neurological deficits at 24 hours and 48 hours postoperatively; the expression levels of LOX-1, NF-κB, ROS , SOD in brain tissues, and the expression levels of inflammatory factors (IL-1α, IL-1β, IL-18, TNF-α) in serum were observed in rats. Results: Compared with the I/R group, short-term exposure to medium and high concentrations of PM2.5 increased the volume of cerebral infarction and aggravated the neurological impairment in ischemia-reperfusion rats (p<0.05), increased the expression levels of inflammatory factors (IL-1α, IL-1β, IL-18, TNF-α) in serum of the I/R rats (p<0.05), inhibited SOD, promoted the expression of ROS, and increased the oxidative stress injury. Moreover, moderate and high PM2.5 exposure significantly up-regulated the protein expression levels of LOX-1 and NF-κB in the brain tissue of ischemia-reperfusion rats (p<0.001). Conclusion: Medium and high PM2.5 exposure increases inflammatory reactions and oxidative stress injury in ischemia-reperfusion rats, exacerbating cerebral infarct volume and neurological impairment. The neurological damaging effects of PM2.5 exposure in I/R rats may be related to its pro-inflammatory and pro-oxidative effects through up-regulation of LOX-1, NF-κB inflammatory mediators.