Abstract
In this study, effects of capsaicin, an active ingredient of the capsicum plant, were investigated on human 5-hydroxytryptamine type 3 (5-HT3) receptors. Capsaicin reversibly inhibited serotonin (5-HT)-induced currents recorded by two-electrode voltage clamp method in Xenopus oocytes. The inhibition was time- and concentration-dependent with an IC50 = 62 μM. The effect of capsaicin was not altered in the presence of capsazepine, and by intracellular BAPTA injections or trans-membrane potential changes. In radio-ligand binding studies, capsaicin did not change the specific binding of the 5-HT3 antagonist [3H]GR65630, indicating that it is a noncompetitive inhibitor of 5-HT3 receptor. In HEK-293 cells, capsaicin inhibited 5-HT3 receptor induced aequorin luminescence with an IC50 of 54 µM and inhibition was not reversed by increasing concentrations of 5-HT. In conclusion, the results indicate that capsaicin acts as a negative allosteric modulator of human 5-HT3 receptors.
Highlights
Capsaicin, a unique alkaloid extracted from Chili peppers of Capsicum family, is responsible for the hot pungent taste of this plant
In the present study, using electrophysiological and biochemical methods, we have investigated the effect of capsaicin on the functional properties of human 5-hydroxytryptamine type 3 (5-HT3) receptors expressed in Xenopus oocytes and HEK-219 cells
Fast inward currents activated by 5-HT (1 mM) or 2-methyl-5-HT (10 mM) were completely inhibited by 0.5 μM MDL72222, a specific 5-HT3 receptor antagonist, indicating that functional 5-HT3 receptors are expressed in Xenopus oocytes (n = 7)
Summary
A unique alkaloid extracted from Chili peppers of Capsicum family, is responsible for the hot pungent taste of this plant. Capsaicin together with dihydrocapsaicin constitute nearly 90% of the capsaicinoid alkaloids found in chili pepper (O’Neill et al, 2012). Therapeutic effects of capsaicin have been gaining increasing interest in various fields of medicine ranging from analgesia, anti-inflammation, and obesity to treatment of cancer (Sharma et al, 2013; Srinivasan, 2016; Patowary et al, 2017; Zhang et al, 2020). TRPV1 is a non-selective, Ca2+ permeable cation channel activated by protons, noxious heat, endogenous lipids, and exogenous ligands, such as resiniferatoxin and capsaicin (Lumpkin and Caterina, 2007; O’Neill et al, 2012). The activation of TRPV1 is considered to be an important mechanism, the exact nature of the widely ranging biological actions of capsaicin is currently unknown
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