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Abstract
In this study, we explored the effects of propofol on oxidative stress response, cytokine secretion, and autophagy in rats with ischemia-reperfusion (I/R) injury and oxygen-glucose deprivation (OGD)-stimulated primary microglia and analyzed the role of the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) pathway in this process. Rat models of I/R injury and OGD models of primary microglia were established. Neurobehavioral scores were evaluated 24h after reperfusion, and oxidative stress indicators, cytokine levels, and autophagy-related markers of rats and OGD-activated primary microglia were evaluated. Activation of the PI3K/Akt pathway was also assessed. The results showed that propofol pretreatment can improve nerve function in rats with I/R injury, inhibit oxidative stress response and inflammatory cytokine secretion, and promote autophagy in rats with I/R injury and OGD-activated primary microglia, and that the PI3K-Akt pathway was activated in this process. Following the addition of a PI3K/Akt pathway inhibitor, the effects of propofol on autophagy in rats with I/R injury and primary microglia were inhibited significantly. The results indicate that propofol promotes autophagy via the PI3K/Akt pathway in cerebral I/R injury.
Published Version
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