Alpinae Oxyphyllae Fructus alleviated LPS‐induced cognitive impairments via PI3K/AKT/NF‐κB signaling pathway. Issue 3 (7th December 2021)

• Record Type: Journal Article
• Authors: Yan, Tingxu; Zhang, Xiaozhuo; Mao, Qianqian; Wu, Bo; He, Bosai; Jia, Ying; Shang, Lei
• Is Part Of: Environmental toxicology. Volume 37:Issue 3(2022)
• Page Start: 489
• Page End: 503
• Publication Date: 2021-12-07
• Subjects: Alpinae Oxyphyllae Fructus -- Alzheimer's disease -- inflammatory cytokines -- LPS -- PI3K/AKT/NF‐κB; Water quality bioassay -- Periodicals; Water -- Pollution -- Toxicology -- Periodicals; Microbiological assay -- Periodicals; Toxicity testing -- Periodicals; Environmental toxicology -- Periodicals; Environmental Pollution -- Periodicals; Environmental Pollutants -- Periodicals; Environmental Monitoring -- Periodicals; Écotoxicologie -- Périodiques; Pollution -- Périodiques; 615.902
• DOI: 10.1002/tox.23415
• Languages: English
• ISSNs: 1520-4081

Abstract

Abstract: Herein, we aim to investigate the effect of Alpinae Oxyphyllae Fructus (AOF) on cognitive impairments and neuroinflammation in a lipopolysaccharide (LPS)‐induced models of AD. Mice were injected intracerebroventricularly with LPS, and then administrated AOF using a gavage for 6 weeks. Spatial working memory was assessed using the Y‐maze and Morris water maze test, whereas the levels of PI3K, AKT, p‐AKT, p‐GSK3β, GSK3β, NF‐κB, IL‐1β, IL‐6, and TNF‐α were evaluated using western blot and ELISA assay. Our data showed that AOF was able to significantly alleviate the memory decline in LPS‐induced AD mice. Moreover, AOF was able to protect neurons through the PI3K/AKT signaling pathway and significantly decrease NF‐κB, IL‐6, IL‐1β, and TNF‐α levels in the hippocampal and cortex tissues, which were reversed through the use of LY294002. Additionally, we discovered that AOF could significantly decrease the high expression of cytokines as well as the expression and translocation of NF‐κB induced by LPS in PC12 cells. These results demonstrate the anti‐neuroinflammatory effect of AOF in both cell and animal models of AD, thereby slowing down the process and development of the disease.