作者: Yuanyuan Li , Chengyu Yin , Xiaojie Li , Boyu Liu , Jie Wang
DOI: 10.3390/IJMS20235917
关键词: TLR4 、 Peripheral neuropathy 、 Pharmacology 、 TRPV1 、 Analgesic 、 Electroacupuncture 、 Dorsal root ganglion 、 Neuropathic pain 、 Microglia 、 Medicine
摘要: Paclitaxel-induced peripheral neuropathy is a common adverse effect during paclitaxel treatment resulting in sensory abnormalities and neuropathic pain chemotherapy cancer survivors. Conventional therapies are usually ineffective possess effects. Here, we examined the effects of electroacupuncture (EA) on rat model paclitaxel-induced related mechanisms. EA robustly persistently alleviated hypersensitivities. Mechanistically, TLR4 (Toll-Like Receptor 4) downstream signaling MyD88 (Myeloid Differentiation Primary Response 88) TRPV1 (Transient Potential Vallinoid 1) were upregulated dorsal root ganglion (DRGs) paclitaxel-treated rats, whereas reduced their overexpression. Ca2+ imaging further indicated that channel activity was enhanced DRG neurons rats suppressed activity. Pharmacological blocking mimics analgesic hypersensitivities, capsaicin reversed EA's effect. Spinal astrocytes microglia activated activation. These results demonstrated alleviates via mechanisms possibly involving suppressing upregulation neurons, which result spinal glia Our work supports as potential alternative therapy for pain.