Decursin Alleviates Mechanical Allodynia in a Paclitaxel-Induced Neuropathic Pain Mouse Model
- Authors
- Son, Dang Bao; Choi, Woosik; Kim, Mingu; Go, Eun Jin; Jeong, Dabeen; Park, Chul-Kyu; Kim, Yong Ho; Lee, Hanki; Suh, Joo-Won
- Issue Date
- Mar-2021
- Publisher
- MDPI
- Keywords
- CINP; decursin; recovery of damaged neuronal network; TRPV1 antagonist; lead compound
- Citation
- CELLS, v.10, no.3
- Journal Title
- CELLS
- Volume
- 10
- Number
- 3
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80637
- DOI
- 10.3390/cells10030547
- ISSN
- 2073-4409
- Abstract
- Chemotherapy-induced neuropathic pain (CINP) is a severe adverse effect of platinum- and taxane-derived anticancer drugs. The pathophysiology of CINP includes damage to neuronal networks and dysregulation of signal transduction due to abnormal Ca2+ levels. Therefore, methods that aid the recovery of neuronal networks could represent a potential treatment for CINP. We developed a mouse model of paclitaxel-induced peripheral neuropathy, representing CINP, to examine whether intrathecal injection of decursin could be effective in treating CINP. We found that decursin reduced capsaicin-induced intracellular Ca2+ levels in F11 cells and stimulated neurite outgrowth in a concentration-dependent manner. Decursin directly reduced mechanical allodynia, and this improvement was even greater with a higher frequency of injections. Subsequently, we investigated whether decursin interacts with the transient receptor potential vanilloid 1 (TRPV1). The web server SwissTargetPrediction predicted that TRPV1 is one of the target proteins that may enable the effective treatment of CINP. Furthermore, we discovered that decursin acts as a TRPV1 antagonist. Therefore, we demonstrated that decursin may be an important compound for the treatment of paclitaxel-induced neuropathic pain that functions via TRPV1 inhibition and recovery of damaged neuronal networks.
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