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21KF-061
TMI-1, TNF-α converting enzyme inhibitor, protect paclitaxel-induced neurotoxicity in the dorsal root ganglion cells
Young-Hoon Jung, Eunsoo Kim, Yesul Kim, Giyoung Yun, Jiseok Baik, Hae-Kyu Kim
Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Yangsan, Republic of Korea1Department of Anesthesia and Pain Medicine, Biomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea2
Background: Chemotherapy-induced peripheral neuropathy (CIPN) gives cancer survivors negative quality of life impacts and a challenge to treat with existing drugs for neuropathic pain. TNF-α is known to potentiate TRPV1 activity, which contributes to CIPN. converting enzyme inhibitor, Here we assessed the role of TMI-1, a TNF-α converting enzyme inhibitor, signaling in paclitaxel (PAC)-induced neurotoxicity in dorsal root ganglion (DRG) cells
Materials and Methods: Immortalized DRG neuronal 50B11 cells were cultured and treated PAC or PAC with TMI-1 following neuronal differentiation. Cell viability, analysis of neurite growth, immunofluorescence, calcium flow cytometry, western blotting, quantitative RT-PCR, and cytokine quantitation by ELISA were performed to examine the role of TMI-1 on neurotoxicity in neuronal cells.
Results: PAC decreased the length of neurites and upregulated expression of TRPV1 in 50B11 cells. TMI-1 showed a protective effect by suppression of inflammatory signaling, especially secretion of TNF-α
Conclusions: TMI-1 shows the partially protective effect of paclitaxel-αinduced neurotoxicity by reversing upregulation of TRPV1 and decreasing inflammatory cytokines including TNF-α, IL-1β, and IL-6 in neuronal cells