Abstract
Capsaicin is a natural compound that produces a warm sensation and is known for its remarkable medicinal properties. Understanding the interaction between capsaicin with lipid membranes is essential to clarify the molecular mechanisms behind its pharmacological and biological effects. In this study, we investigated the effect of capsaicin on thermoresponsiveness, fluidity, and phase separation of liposomal membranes. Liposomal membranes are a bioinspired technology that can be exploited to understand biological mechanisms. We have shown that by increasing thermo-induced membrane excess area, capsaicin promoted membrane fluctuation. The effect of capsaicin on membrane fluidity was dependent on lipid composition. Capsaicin increased fluidity of (1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membranes, while it rigidified DOPC and cholesterol-based liposomes. In addition, capsaicin tended to decrease phase separation of heterogeneous liposomes, inducing homogeneity. We imagine this lipid re-organization to be associated with the physiological warming sensation upon consumption of capsaicin. Since capsaicin has been reported to have biological properties such as antimicrobial and as antiplatelet, the results will help unravel these biological properties.
Highlights
Capsaicin (8-methyl-N-vanillyl-trans-6-nonenamide) is a chemosensory molecule derived from chili peppers of the Capsicum plant
We have demonstrated that capsaicin increased thermoresponsiveness of DOPC/Chol liposomal membranes
The inclusion of capsaicin resulted in greater thermo-induced membrane excess area, thereby prompting liposomes to fluctuate more upon increasing temperature
Summary
Capsaicin (8-methyl-N-vanillyl-trans-6-nonenamide) is a chemosensory molecule derived from chili peppers of the Capsicum plant. It exhibits analgesic [1] and inflammatory properties [2], used to mitigate neurogenic pain and cure rheumatoid arthritis [3]. The exposure of nociceptor terminals to capsaicin leads to excitation of neurons and consequent perception of pain and local release of inflammatory mediators. Nociceptor terminals become insensitive to capsaicin, as well as to other noxious stimuli [10]. The long-term loss of responsiveness can be explained by the death of the nociceptor or destruction of its peripheral terminals following exposure to capsaicin [11]
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