Activation of G protein-coupled receptor 39 alleviates neuropathic pain and chronic inflammation.

Neuropathic pain (NP) is mainly caused by lesions or diseases of the somatosensory nervous system and triggers severe physical burdens to patients. It is claimed that activated microglia-mediated neuroinflammation participates in the development of NP, which is regulated by p38 mitogen-activated protein kinase (MAPK)/nuclear factor-κappa B (NF-κB) p65 signaling. G protein-coupled receptor 39 (GPR39) is a trans-membrane protein involved in the activation of cellular transduction pathways, and TC-G 1008, a GPR39 agonist, is believed to have inhibitory effects on neuroinflammation.

Propofol alleviates neuropathic pain in chronic constriction injury rat models via the microRNA-140-3p/Jagged-1 peptide/Notch signaling pathway.

Chronic constriction injury (CCI) of the sciatic nerve was used to establish neuropathic pain (NP) models in rats. CCI rats were then treated with propofol (Pro) and their paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured. In addition, the expression patterns of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10 were detected.

Agomelatine Attenuates Isoflurane-Induced Inflammation and Damage in Brain Endothelial Cells.

Background And Purpose: Neurotoxicity of anesthetics has been widely observed by clinicians. It is reported that inflammation and oxidative stress are involved in the pathological process. In the present study, we aimed to assess the therapeutic effects of agomelatine against isoflurane-induced inflammation and damage to brain endothelial cells.

Radiotherapy Suppresses Bone Cancer Pain through Inhibiting Activation of cAMP Signaling in Rat Dorsal Root Ganglion and Spinal Cord.

Radiotherapy is one of the major clinical approaches for treatment of bone cancer pain. Activation of cAMP-PKA signaling pathway plays important roles in bone cancer pain. Here, we examined the effects of radiotherapy on bone cancer pain and accompanying abnormal activation of cAMP-PKA signaling.