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

Autophagy is a lysosomemediated cell contentdependent 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 LPSinduced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)1beta and tumor necrosis factor (TNF)alpha was analyzed using ELISAs, and the expression levels of the autophagy marker microtubuleassociated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL1beta and TNFalpha and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3kinase (PI3K), phosphorylated protein kinase B (pAKT), and phosphorylated mammalian target of rapamycin (pmTOR). The present results suggest that ligustrazine improved LPSinduced 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.