神经毒性
氧化应激
药理学
小胶质细胞
脂质过氧化
毒性
化学
体内
炎症
抗氧化剂
谷胱甘肽
神经炎症
医学
生物化学
内科学
生物
酶
生物技术
有机化学
作者
Teng-Teng Ren,Jiaying Yang,Jun Wang,Sheng-Rui Fan,Rongfeng Lan,Xiaoyan Qin
标识
DOI:10.1007/s00011-021-01513-7
摘要
OBJECTIVE Gisenoside Rg1 is a potent neuroprotectant in ginseng. The aim of this study was to investigate the elimination effect of Rg1 on cadmium (Cd)-induced neurotoxicity. MATERIALS AND METHODS A cumulative Cd exposure mouse model was established. Also, the toxicity of Cd and the protective effect of Rg1 were examined in vitro using cultured neurons and microglia. RESULTS We found that Cd-intoxicated mice exhibited significant injury in the liver, kidney, small intestine, and testis, along with cognitive impairment. Antioxidant enzymes such as SOD, GSH-Px and CAT were reduced in the blood and brain, and correspondingly, the lipid peroxidation product MDA was elevated. In the brain, astrocytes and microglia were activated, characterized by an increase in inflammatory factors such as TNF-α, IL-1β and IL-6, as well as their protein markers GFAP and IBA1. However, Rg1 eliminated Cd-induced toxicity and restored oxidative stress and inflammatory responses, correspondingly restoring the behavioral performance of the animals. Meanwhile, the BDNF-TrkB/Akt and Notch/HES-1 signaling axes were involved in the Rg1-mediated elimination of Cd-induced toxicity. CONCLUSION Rg1 is a promising agent for the elimination of Cd-induced toxicity.
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