Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway.
作者： Guangming Li , Sisi Liu , Huili Wang , Rui Pan , Haijie Tang
关键词: PI3K/AKT/mTOR pathway 、 Tumor necrosis factor alpha 、 Neuroinflammation 、 Protein kinase B 、 Interleukin 、 Cancer research 、 Medicine 、 Autophagy 、 Inflammation 、 Molecular medicine
摘要: 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 lipopolysaccharide (LPS)‑induced brain and effects traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment rats. Furthermore, molecular mechanisms by which influences impairments were explored. The production inflammatory mediators interleukin (IL)‑1β tumor necrosis factor (TNF)‑α was analyzed using ELISAs, expression levels marker microtubule‑associated protein light chain 3 (LC3) II/I western blotting. LPS exposure upregulated IL‑1β TNF‑α downregulated LC3 II/I. Ligustrazine activated preventing phosphoinositide 3‑kinase (PI3K), phosphorylated kinase B (p‑AKT), mammalian target rapamycin (p‑mTOR). present results suggest improved activating ameliorated neuronal injury regulating PI3K/AKT/mTOR signaling pathway. These findings provide important reference for prevention treatment neuroinflammation.
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