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.