Caffeic acid phenethyl ester reversed cadmium-induced cell death in hippocampus and cortex and subsequent cognitive disorders in mice: Involvements of AMPK/SIRT1 pathway and amyloid-tau-neuroinflammation axis. (October 2020)

• Record Type: Journal Article
• Authors: Hao, Rili; Song, Xinyu; Li, Feng; Tan, Xintong; Sun-Waterhouse, Dongxiao; Li, Dapeng
• Is Part Of: Food and chemical toxicology. Volume 144(2020)
• Publication Date: 2020-10
• Subjects: Cadmium -- Caffeic acid phenethyl ester -- Neurotoxicity -- Inflammation -- Apoptosis; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2020.111636
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: Exposure to nonbiodegradable cadmium (Cd) causes many health problems including the damage to the nervous system. This study aimed to increase knowledge about its neurotoxic effects and the neuroprotective potential of caffeic acid phenethyl ester (CAPE, a polyphenol abundant in honeybee propolis). In mice, CAPE (10 μmol/kg/day body weight) attenuated significantly learning and memory deficits induced by CdCl2 (1.5 mg/kg/day body weight). For the CdCl2 -treated mice, CAPE increased crossing number in open field test, decreased the alternation in Y-maze test, and increased the latency time and error number in step down test. CAPE also inhibited CdCl2 -initiated Aβ accumulation and activation of pro-inflammatory factors and microglia in the brains. Therefore, CAPE could be a food-derived neuroprotective agent against Cd-induced neurotoxicity and neurodegenerative disorders, through attenuating neuronal apoptosis and neuroinflammation via the AMPK/SIRT1 pathway and amyloid-tau-neuroinflammation axis. Graphical abstract: Image 1 Highlights: CAPE has protective effect on CdCl2 -induced neurotoxicity and neurodegenerative disorders. CAPE plays a protective role through attenuating neuronal apoptosis and neuroinflammation. AMPK/SIRT1 pathway and amyloid-tau-neuroinflammation axis involve in the protection of CAPE.