异甘草素
小胶质细胞
神经病理性疼痛
MAPK/ERK通路
炎症
信号转导
医学
转录因子
药理学
化学
细胞生物学
生物
免疫学
基因
生物化学
作者
Zikun Wang,Shu Jia,Xiaozheng Kang,Shang Chen,L. Zhang,Z. Tian,Xiao Liang,Chunyang Meng
标识
DOI:10.1016/j.intimp.2024.113536
摘要
The analgesic effect of ISL on neuropathic pain primarily stems from its ability to inhibit the activation of spinal microglia and neuroinflammation. This mechanism may be attributed to the capacity of ISL to suppress microglial activation, reduce the expression of pro-inflammatory cytokines by inhibiting the ERK signaling pathway, and decrease transcriptional expression of CEBPB.
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