Ligustrazine ameliorates lipopolysaccharide-induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway

Autophagy is a lysosome-mediated cell content- dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)-induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS-induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)-1β and tumor necrosis factor (TNF)-α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule-associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL-1β and TNF-α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR). The present results suggest that ligustrazine improved LPS-induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.