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At least 19 recordsLinked to original sources
PubMed1976

Sensory effects of capsaicin congeners. Part II: Importance of chemical structure and pungency in desensitizing activity of capsaicin-type compounds.

The characteristic insensitivity of sensory nerve endings to chemically induced pain brought about by capsaicin could be reproduced on the rat's eye by pungent vanillylamides, homovanilloyl-alkylamides and piperine, while homovanilloyl-cycloalkylamides, -azacycloalkylamides, - alkylesters, -alkyl-homovanillylamides, undecenoyl-3-aminopropranololand zingerone were practically ineffective in this respect. Desensitizing potency was not parallel with the stimulating effect of the compounds, e.g. the strongly pungent homovanilloyl-octylester failed to desensitize the receptors, while the less pungent homovanilloyl-dodecylamide proved to be a more potent desensitizing agent than capsaicin itself. It is concluded that the inverse position of the acylamide linkage does not modify, while its replacement by an esteric group completely abolishes the desensitizing activity. In contrast to the stimulating effect, in desensitizing action the presence of an alkyl chain is essential and its optimal length corresponds to 10-12 C atoms. On the basis of these results the possible molecular interactions at the site of action are discussed.

Animals↗
PubMed2026

Capsaicin ameliorates glycemic levels via gut microbiota-derived 5-aminolevulinic acid in mice.

BACKGROUND: Capsaicin, a natural alkaloid in chili peppers, regulates glycemic levels; however, its mechanisms and therapeutic potential remain unclear. This study aimed to elucidate the role of gut microbiota and their metabolites in mediating capsaicin's glycemic regulatory effects. We conducted experiments in specific pathogen-free (SPF) and germ-free (GF) mice, transient receptor potential vanilloid 1 (TRPV1) receptor ablation studies, and fecal microbiota transplantation (FMT) to demonstrate the involvement of gut microbiota in capsaicin-mediated glycemic control. Metagenomics and metabolomics analyses were employed to identify key microbial strains and metabolic pathways. Keystone strains and metabolites were supplemented in GF mice without capsaicin intervention to validate their effects on glycemic regulation. In vitro co-culture experiments were performed to investigate the mutualistic relationships among keystone strains under capsaicin treatment. RESULTS: Gut microbiota constitute an important component of capsaicin-mediated glycemic regulation, acting in concert with but not solely dependent on TRPV1 signaling. Gut microbiota altered by capsaicin promote the production of 5-aminolevulinic acid (5-ALA), which contributes to heme synthesis and enhances glycemic control. Supplementation with Akkermansia muciniphila, Ligilactobacillus murinus, or 5-ALA in GF mice recapitulates the glycemic benefits of capsaicin. Furthermore, capsaicin enriches Akkermansia muciniphila, which in turn supports the growth of Ligilactobacillus murinus. CONCLUSION: Capsaicin-induced changes in the gut microbiota promote 5-ALA synthesis, leading to improved glycemic control. These findings suggest that dietary or probiotic interventions targeting gut microbiota, particularly Akkermansia muciniphila and 5-ALA, may offer promising strategies for managing glycemic disorders, including type 2 diabetes (T2D). Video Abstract.

Animals↗
PubMed1977

The effect of capsaicin on the adenylate cyclase activity of rat brain.

The effect of capsaicin on the adenylate cyclase activity in different regions of the rat brain (preoptic area of the hypothalamus, cerebral cortex and cerebellum) was investigated. Capsaicin added in vitro (10(-7)-10(-5) M) increased the adenylate cyclase activity of different brain regions. Following systemic capsaicin desensitization adenylate cyclase activity was significantly increased in the preoptic area. The enhanced adenylate cyclase activity in the preoptic area was inhibited by the vitro addition of capsaicin or 5-HT, whereas desensitization did not affect the in vitro activating effect of capsaicin in other brain regions (cerebral cortex, cerebellum). It is assumed that the pharmacological effect of capsaicin in the preoptic area is mediated through the activation of adenylate cyclase. Since capsaicin induces irreversible impairment of the function of warmsensitive hypothalamic neurons it is assumed that adenylate cyclase is involved in maintaining normal thermoregulatory functions.

Adenylyl Cyclases↗
PubMed1979

Effect of capsaicin on gastric acid secretion and mucosal blood flow in the rat.

The effect of capsaicin, a pungent ingredient in capsicum fruit, upon gastric acid secretion and mucosal blood flow was assessed in the anesthetized rat. At each 15 minute interval, 0.3 ml saline solution, with or without various doses of pure synthetic capsaicin (the doses varied from 50 to 2,000 microgram/kg rat) was delivered into the gastric lumen via a gastric fistula. The gastric contents were withdrawn after 15 minutes for acid assay and replaced with a new saline solution. Capsaicin of increasing doses (up to 1,000 microgram/kg) progressively increased the acid output. Gastric inhibitors hexamethonium and atropine, completely abolished the acid secretion induced by capsaicin whereas secretin only partially reduced such a response. The systemic blood pressure was not affected by the capsaicin or the method employed. However, the aminopyrine clearance which was the indicator of the gastric mucosal blood flow increased in accordance with the increase in the acid output. It is suggested that the effect of capsaicin on the acid secretion and mucosal blood flow is by the release of endogenous gastric secretagogues which increase both tissue perfusion and the secretory activity.

Aminopyrine↗
PubMed1977

[Effects of capsaicin on spontaneous unit discharges in medial thalamic single neurons of cats (author's transl)].

The effect of capsaicin was studied in gallamine triethiodide immobilized adult cats. Single neurons were recorded from the medial thalamus with a stainless steel microelectrode. Out of 21 neurons recorded in this experiment, 10 were responsive to both nociceptive (pinch) and non-nociceptive (hair bending and/or tapping) stimuli. Six neurons were responsive to only non-nociceptive stimuli and 5 were not responsive to these stimuli. Out of 10 neurons responding to both nociceptive and non-nociceptive stimuli, 9 were responsive to both bradykinin (3 microgram) and capsaicin (3 microgram). Out of 6 neurons responding to only non-nociceptive stimuli, 5 were not responsive to either bradykinin and capsaicin. All neurons responding to bradykinin were also responsive to capsaicin. The latency for bradykinin and capsaicin was 7.64 +/- 1.12 sec and 0.97 +/- 0.07 sec, respectively. The increased in firing frequency produced by capsaicin was depressed by morphine. However, these depressant effects of morphine on single unit activity were antagonized by naloxone.

Action Potentials↗
PubMed1979

Nociceptive threshold after neonatal capsaicin treatment.

The nociceptive threshold as determined by the reaction time in the hot-plate and tail-flick tests was measured 3 to 4 months after pretreatment of young rats with capsaicin (50 mg kg-1 s.c.). The reaction time in the tail-flick test was prolonged in rats pretreated with capsaicin on the 2nd day of life. Capsaicin pretreatment up to the 10th day of life also resulted in a prolonged reaction time in the hot-plate test whereas capsaicin pretreatment after the 10th day of life was without effect. The elevation of the nociceptive threshold after neonatal capsaicin pretreatment most likely follows from degeneration of afferent nerve fibres activated by noxious stimuli.

Animals↗
PubMed1979

Reflex bronchoconstriction induced by capsaicin in the dog.

To determine whether receptors stimulated by the injection of capsaicin into the pulmonary circulation cause reflex changes in airway size, six dogs were anesthetized with chloralose, paralyzed with succinylcholine, and mechanically ventilated (2 cm H2O PEEP). Intrapulmonary airways were outlined with tantalum dust, and diameters were determined by taking serial roentgenograms at end expiration. Capsaicin (20 micrograms/kg) injected into the right ventricle significantly decreased airway diameter (20%), heart rate, aortic pressure, and pulmonary artery pressure. In contrast, capsaicin injected into the left ventricle did not alter airway diameter or aortic pressure, although heart rate and pulmonary artery pressure decreased but to a lesser extent than after right ventricular injection. After vagotomy, capsaicin had no effect on airway diameter or heart rate but aortic pressure and pulmonary artery pressure increased slightly. Results suggest that pulmonary receptors sensitive to capsaicin and accessible via the pulmonary circulation produce reflex bronchoconstriction. One possible function of this vagal reflex is to assist fluid movement from microvasculature to peribronchial space by reducing peribronchial pressure.

Animals↗
PubMed1979

Capsaicin-sensitive innervation of the guinea-pig taenia caeci.

1. Stimulation (2--50 Hz) of the mesenteric nerves of the guinea-pig taenia caeci gave rise to contraction of the muscle obtained from animals pretreated with the adrenergic neuron-blocking agent guanethidine. Contraction was the response to stimulation at low frequencies (2--5 Hz) in about half of the untreated preparations as well. 2. The response was abolished by hyocine (4.5 x 10(-7) M), but was unaffected by the ganglionic blocking agent mecamylamine (4.9 x 10(-5) M). Physostigmine (2.4 x 10(-8) M) enhanced the contractions. 3. Capsaicin (9.8 x10(-6) M) elicited a contraction of the taenia caeci followed by a long-lasting tachyphylaxis. Contraction in response to stimulation of the mesenteric nerves was absent after this pretreatment. 4. Neither the response to direct excitation of the cholinergic neural elements of the myenteric plexus, nor the relaxation caused by stimulation of adrenergic fibres were influenced by capsaicin. "Purinergic" relaxation produced by field stimulation (0.5--10 Hz) remained also unchanged. 5. No functional evidence has been found for the presence of parasympathetic preganglionic fibres among the perivascular nerves applying the taenia. 6. It is concluded that capsaicin-sensitive nerves excite cholinergic neurons of the myenteric plexus.

Animals↗
PubMed1979

Simultaneous microdetermination of capsaicin and its four analogues by using high-performance liquid chromatography and gas chromatography--mass spectrometry.

An improved method is described for the simultaneous determination of capsaicin and its analogues at levels from nanograms to micrograms using high-performance liquid chromatography (HPLC) and gas chromatography--mass spectrometry. This method consists of two steps: firstly, purification and determination of total capsaicinoid by HPLC, and secondly, the simultaneous determination of capsaicin and its analogues by mass chromatography (MC) or mass fragmentography (MF). Crude extracts of capsaicinoid were purified with a Zorbax SIL column. Total capsaicinoid was detected at 235 nm and measured automatically by a microcomputer. It was collected, evaporated, trimethylsilylated and subjected to MC or MF. After monitoring the molecular ions of trimethylsilyl derivatives of capsaicinoid and the internal standard, the absolute contents of each analogue were determined by computer. By using this method, capsaicin and all of its analogues can be determined simultaneously at levels from micrograms to nanograms without any interferences from other components.

Capsaicin↗
PubMed1977

Modification by capsaicin and compound 48/80 of dye leakage induced by irritants in the rat.

Concentration-related dye leakage produced by intracutaneous injections of irritants was measured in rats by an Evans blue technique. 2 In rats pretreated with a total dose of 50 mg capasaicin over 4 days, the response to capsaicin, formalin, HCl, KCl, prostaglandin E1, bradykinin and bradykinin with prostglandin E1 (10(-6) M) were greatly reduced, the responses to histamine and 5-hydroxytryptamine were slightly reduced and those to adenosine 5'-triphosphate (ATP) and compound 48/80 were unaffected. 3 Pretreatment with intracutaneous injections of compound 48/80 (0.5 mug, 24 and 48 h previously) recuded the responses to ATP, compound 48/80, HCl, KCl, prostaglandin E1, and bradykinin but did not affect those to histamine, 5-hydroxytryptamine or bradykinin with prostaglandin E1 (10(-6) M). 4 Responses to capsaicin and formalin produced spotted blueing extending over a large area and were suppressed by compound 48/80 in the smaller pretreated area only. Capsaicin responses were reduced with larger doses of compound 48/80 (total dose 15 mug). 5 It is concluded that the production of neurogenic oedema involves both sensory nerves and mast cells.

Adenosine Triphosphate↗
PubMed1977

Effect of capsaicin on electrical slow waves in the isolated cat colon.

Because of the laxative effect of capsaicin, we examined the effect of that agent on the electromyogram of the isolated cat colon. At a concentration of 10(-4)M, it caused a significant reduction in the frequency of the electrical slow waves in the proximal half of the colon. Frequency fell to its lowest value, 45% of control (P less than 0-001), in the most proximal 10% of the organ below the ileocecal junction, and the effect progressively diminished along the colon. In the distal half of the colon, the change in frequency was not significant. Sectioning of the colon into segments reduced the frequency of the slow waves in the proximal half of the colon, and capsaicin, in a concentration of 10(-4)M, further reduced the frequency in the segments representing the proximal 30% of the colon. This effect of capsaicin is like that reported previously with other laxative agents.

Animals↗
PubMed1978

Selective degeneration of chemosensitive primary sensory neurones induced by capsaicin: glial changes.

Capsaicin treatment of newborn rats results in the degeneration of primary sensory neurones involved in the mediation of chemogenic pain. In the present study glial changes following the pharmacologically-induced degeneration of unmyelinated primary afferent fibres terminating in Rexed's laminae I and II of the spinal cord were investigated. Light microscopy revealed an increase in the number of phagocytic glial cells in this area, reaching a maximum at 24 h after the administration of capsaicin; they had almost completely disappeared by 72 h. At the ultrastructural level these cells were characterized by their elongate or irregular nuclei with a pronounced heterochromatin pattern, a moderately dense cytoplasmic matrix, hour-glass shaped mitochondria and very large numbers of heterogeneous dense bodies and lipid droplets. On the basis of these observations, these cells were considered to represent reactive microglial cells engaged in the phagocytosis of degenerated neuronal debris. The possible origin and mode of elimination of these elements from the central nervous tissue is briefly discussed.

Animals↗
PubMed1979

Salivary cooling, escape reaction and heat pain in capsaicin-desensitized rats.

Salivary thermolytic mechanisms (weight of salivary glands, effect of desalivation on water intake and body temperature, grooming activity) as well as escape behaviour and reaction to heat pain were studied in capsaicin-desensitized and control rats exposed to various warm ambient temperatures. Body temperature of the desensitized rats increased more than the controls' at all the ambient temperatures studied (32, 34 and 36 degrees C); however, significant differences in the mechanism of salivary cooling were obtained only at 34 and 36 degrees C. Central impairment of saliva spreading in desensitized rats seems evident. Complete surgical desalivation did not increase hyperthermia of control and desensitized animals in warm environments. Therefore other mechanisms, primarily vasodilatatory, must also be involved in the rat's thermolytic normal response. Although desensitized rats did not show a tendency to escape from the warm environment their response to heat pain was normal. In conclusion, it is suggested that heat perception in desensitized animals is impaired; however, the existence of some capsaicin-insensitive thermolytic mechanisms (prone extension of the body) cannot be excluded.

Animals↗
PubMed2026

Faster N1 latency in response to homeostatic-like plasticity of PREPs is impaired during pain: A randomized-placebo capsaicin-pain study.

INTRODUCTION: Homeostatic-like plasticity (HP-like) stabilizes cortical excitability through long-term potentiation and depression-like mechanisms. The efficacy of homeostatic regulation in the corticomotor system is impaired during pain, which may have functional relevance for chronic pain. This study investigated whether a cortical HP-like response could be assessed by nociceptive stimulation, and if such response was impaired by experimental tonic pain. METHODS: Twenty-eight healthy participants completed placebo and capsaicin sessions, with 11 sham controls for time and design. HP-like plasticity was induced with two blocks of anodal tDCS over the primary motor cortex. The N1 (TP7) and N2P2 (Cz) components of electrically induced pain-related evoked potentials (PREPs) were assessed from the volar forearm before and after patch application, and again immediately and 20 min after HP-like induction. An HP-like response was defined by PREP decrease after induction, and further normalization to baseline. RESULTS: Anodal tDCS did not induce an HP-like regulation of PREP amplitudes. Interestingly, an HP-like response was observed as a fastening of N1 latency after HP-like induction, which returned to baseline values after 20 min. The latter effect was impaired during capsaicin-induced pain, where N1 was slower. The N2P2 component showed habituation over time in all sessions. CONCLUSION: This is the first study that investigates the HP-like regulation of nociceptive-evoked responses. An HP-like response was observed as a shortening of N1 latency, suggesting that early nociceptive processing may be susceptible to homeostatic regulation. In contrast, the later component, N2P2, showed habituation over time, which prevented evaluation of HP-like effects.

Humans↗
PubMed1976

Quantitative microanalysis of capsaicin, dihydrocapsaicin and nordihyrocapsaicin using mass fragmentography.

A mass fragmentographic method for the quantitative microanalysis of capsaicin, dihydrocapsaicin and nordihydrocapsaicin in the fruits of Capsicum annuum has been developed. The molecular ions at m/e 377, 379 and 365 in the mass spectra were used for monitoring the trimethylsilyl derivatives of capsaicin, dihydrocapsaicin and nordihydrocapsaicin, respectively. The ratios of the height of each molecular ion to that of an internal standard (cholestane) were linear over the range 5-60 ng. The purification of individual capsaicinoids by high-performance liquid, thin-layer and gas-liquid chromatography is also described.

Capsaicin↗
PubMed1979

Endotoxin fever in capsaicin treated rats.

The fever elicited by 10 micrograms/kg intravenous E. coli endotoxin was significantly higher in capsaicin desensitized rats than in controls, but there was an upper limit to the rise in body temperature in both groups. Capsaicin desensitization permitted the participation of various heat producing mechanisms even if the initial body temperature was high. The fever course was characteristically biphasic, similar as in control rats, thus desensitization did not alter the factors mediating the various phases of the endotoxin response.

Adipose Tissue, Brown↗