Gisenoside Rg1 attenuates cadmium-induced neurotoxicity in vitro and in vivo by attenuating oxidative stress and inflammation

Gisenoside Rg1 attenuates cadmium-induced neurotoxicity in vitro and in vivo by attenuating oxidative stress and inflammation
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Gisenoside Rg1 通过减轻氧化应激和炎症来减轻镉诱导的体外和体内神经毒性

DOI:
10.1007/s00011-021-01513-7
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发表时间:
2021-10-18
影响因子:
6.7
通讯作者:
Qin, Xiao-Yan
Qin, Xiao-Yan
中科院分区:
医学2区
文献类型:
--
作者:
Ren, Teng-Teng;Yang, Jia-Ying;Qin, Xiao-Yan

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人参皂苷Rg1是人参中一种有效的神经保护剂。本研究旨在探讨人参皂甙Rg1对镉(Cd)神经毒性的消除作用。此外,镉的毒性和Rg1的保护作用进行了研究,在体外培养的神经元和小胶质细胞。ResultsWe发现,镉中毒小鼠表现出显着的损伤,在肝脏,肾脏,小肠,睾丸,沿着与认知障碍。血液和脑组织中SOD、GSH-Px、CAT等抗氧化酶活性降低,相应的脂质过氧化产物MDA升高。在大脑中,星形胶质细胞和小胶质细胞被激活,其特征在于炎症因子如TNF-α、IL-1 β和IL-6及其蛋白质标记物GFAP和IBA1的增加。然而,Rg1消除了镉诱导的毒性,恢复了氧化应激和炎症反应,相应地恢复了动物的行为表现。结论Rg1是一种有前途的镉毒性消除剂,其作用机制可能与BDNF-TrkB/Akt和Notch/HES-1信号通路有关。
ObjectiveGisenoside 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 methodsA 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.ResultsWe 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.ConclusionRg1 is a promising agent for the elimination of Cd-induced toxicity.