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Upregulated TNF-α and lactate following ERK-SGK1 activation in the spinal dorsal horn underlies chronic postsurgical pain

1 School of Medical Technology and Nursing, Shenzhen Polytechnic, Shenzhen, Guangdong, China
2 Affiliated Shenzhen Maternity and Child Healthcare Hospital, Southern Medical University, Shenzhen, Guangdong, China
3 Department of Neurology, Xiehe Shenzhen Hospital, Huazhong University of Science and Technology, Shenzhen, Guangdong, China
4 Shenzhen Eye Hospital, Shenzhen, Guangdong, China

Correspondence Address:
Yuying Li,
7098, Liuxian Street, Shenzhen 518055, Guangdong
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cjop.CJOP-D-22-00085

Skin/muscle incision and retraction (SMIR) during surgeries can lead to chronic postsurgical pain (CPSP). The underlying mechanisms are still unclear. In the present study, we showed that SMIR of the thigh induced phosphorylation of extracellular signal-regulated kinase (ERK), followed by serum- and glucocorticoid-inducible kinase-1 (SGK1) activation in the spinal dorsal horn. Intrathecal injection of PD98059, an ERK inhibitor, or GSK650394, a SGK1 inhibitor, significantly attenuated mechanical pain hypersensitivity in SMIR rats. The level of tumor necrosis factor α and lactate in spinal cord was significantly decreased by PD98059 or GSK650394 injection. Furthermore, PD98059 decreased the activation of SGK1 in the spinal dorsal horn. These results indicate that ERK-SGK1 activation followed by proinflammatory mediator release in the spinal dorsal horn underlies CPSP.

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