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- W4377029408 abstract "<b>Abstract ID 16855</b> <b>Poster Board 372</b> Transient Receptor Potential Ankyrin 1 (TRPA1) and Vanilloid 1 (TRPV1) are nociceptive ion channels involving in pain sensation and development of neurogenic inflammation. These non-selective channels are located in the lipid rafts, the cholesterol-rich membrane domains of the plasma membrane of primary sensory neurons and peripheral nerve terminals. Cyclodextrins (CDs) are able to form inclusion complexes with cholesterol and deplete it from lipid rafts. We have already described that lipid raft disruption by Methyl-β-cyclodextrin (MCD) inhibited TRP ion channel function and has analgesic effect in animal models. We tested five different CD derivatives (Randomly methylated β-cyclodextrin: RAMEB, (2-Hydroxypropyl)-γ-cyclodextrin: HPGCD, (2-Hydroxyproyil)-β-cyclodextrin: HPBCD, Sulfobutylated β-cyclodextrin sodium salt: SBECD and (2-Hydroxy-3-N,N,N-trimethylamino) propyl-β cyclodextrin: QABCD; CycloLab Ltd.) in respect of their cytotoxicity (1, 3, 10, 50, 100 mM; 24 h) on chinese hamster ovary (CHO) cells with CellTiter-Glo® Luminescent Cell Viability Assay. MitoTracker™ Red CMXRos fluorescent dye was used to reveal the effect of 24-hour CD treatment on mitochondrial functioning of CHO cells. We performed radioactive <sup>45</sup>Ca<sup>2+</sup>-uptake measurements on TRPA1 and TRPV1 receptor-expressing CHO cells to detect alterations in receptor activation after CD treatment. In CellTiter-Glo® Luminescent Cell Viability Assay the methylated derivative RAMEB showed significant cytotoxic effect in 3.5 mM concentration, but none of the non-methylated derivatives decreased cell viability in 10 mM concentration. HPBCD treatment (1 mM and 10 mM) and QABCD treatment (10 mM) resulted in significantly increased fluorescence intensities of CHO cells’ mitochondria labeled with MitoTracker™ Red CMXRos. All of the investigated CDs were able to inhibit the <sup>45</sup>Ca<sup>2+</sup>-uptake in TRPA1 and TRPV1 receptor-expressing CHO cells in a concentration dependent manner. In conclusion, non-methylated derivatives have much lower cytotoxicity compared to RAMEB. HPBCD and QABCD affected significantly the mitochondrial function and all investigated CD derivatives were able to inhibit TRPA1 and TRPV1 channel activation, presumably via the disruption of lipid rafts. Targeting hydrophobic interactions of the protein-lipid interface might be promising as a novel mechanism of action in analgesia. <b>Support/Funding Information:</b> TKP2021-EGA-16, TKP2021-EGA-13, NKFIH-138936, RRF-2.3.1-21-2022-00015, KTIA_NAP_20017-1.2.1-NKP-2017-00002, ÚNKP-21-3-II New National Excellence Program of the Ministry for Innovation and Technology, Gedeon Richter Talentum Foundation" @default.
- W4377029408 created "2023-05-19" @default.
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- W4377029408 date "2023-05-18" @default.
- W4377029408 modified "2023-10-17" @default.
- W4377029408 title "Cyclodextrins decrease TRPV1 and TRPA1 ion channel activation via lipid raft disruption" @default.
- W4377029408 doi "https://doi.org/10.1124/jpet.122.168550" @default.
- W4377029408 hasPublicationYear "2023" @default.
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