MAPK/ERK通路
神经病理性疼痛
周围神经损伤
小胶质细胞
医学
磷酸化
神经损伤
蛋白激酶A
激酶
神经科学
细胞外
细胞生物学
药理学
麻醉
内科学
生物
坐骨神经
炎症
标识
DOI:10.1517/14728222.9.4.699
摘要
Peripheral nerve injury produces neuropathic pain as well as phosphorylation of mitogen activated protein kinase (MAPK) family in dorsal root ganglia (DRG) and dorsal horn. Following nerve injury, phosphorylation of extracellular signal-regulated protein kinase (ERK), an important member of this family, is sequentially increased in neurons, microglia and astrocytes of the dorsal horn and gracile nucleus, and in injured large DRG neurons. Nerve injury-induced phosphorylation of ERK occurs early and is long-lasting. In several animal models of neuropathic pain, MEK inhibitors, known to suppress the synthesis of ERK, have proven effective to alleviate pain at various time points. Thus, the regulation of ERK/MAPK can be considered as a promising therapeutic target for the treatment of neuropathic pain.
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