神经毒性
黑质
化学
酪氨酸羟化酶
神经保护
免疫印迹
纹状体
体内
多巴胺
p38丝裂原活化蛋白激酶
药理学
生物化学
生物
毒性
信号转导
内分泌学
MAPK/ERK通路
多巴胺能
基因
酶
有机化学
生物技术
作者
Yu-Fei Pang,Jingxin Chen,Jianjun Yang,Yanzhong Xue,Hua Gao,Qinghan Gao
出处
期刊:Food & Function
[Royal Society of Chemistry]
日期:2023-01-01
卷期号:14 (10): 4552-4568
被引量:7
摘要
, LRP improved exploratory and locomotor deficits in ACR-induced rats. LRP activated the Nrf2 pathway in the striatum and substantia nigra. LRP treatment attenuated striatal ROS levels and increased GSH and SOD in ACR-induced rats. Immunohistochemistry, western blot, and ELISA revealed a significant increase in tyrosine hydroxylase (TH) neurons and dopamine and its metabolites in the striatum and substantia nigra under the protective effect of LRP. Therefore, LRP can be a protective agent against ACR-induced brain damage.
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