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| 21KF-061 |
TMI-1, TNF-α converting enzyme inhibitor, protect paclitaxel-induced neurotoxicity in the dorsal root ganglion cells
Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Yangsan, Republic of Korea1 , Department 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
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
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