Gotowe bibliografie tematyczne / Capsaicin Physiological effect

Gotowa bibliografia na temat „Capsaicin Physiological effect”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 31 stycznia 2023

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych

Wybierz rodzaj źródła:

Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Capsaicin Physiological effect”.

Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.

Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.

Artykuły w czasopismach na temat "Capsaicin Physiological effect"

Li, Xi Hong, Gui Ming Lei i Xia Liu. "Effect of Capsaicin-Coated PE Film on Microbiological and Physiological Properties of Rice during Storage". Advanced Materials Research 156-157 (październik 2010): 1109–12. http://dx.doi.org/10.4028/www.scientific.net/amr.156-157.1109.

Pełny tekst źródła

Streszczenie:

Three repellent coated PE film were development for avoiding storage insects and microorganisms. In this work, the microbiological and physiological properties of tetramethrin, cymperator and capsaicin-coated PE packing for rice grain were investigated. The results showed that the capsaicin-coated PE film was the optimal packaging material to preserve rice grain fresh. After three months storage of rice grain, capsaicin-coated PE inhibited the growth of bacteria and fungi than blank-coated PE, and had the similarly inhibiting roles than potent synthetic insecticide-coated PE packing. Especially, free fatty acid content increasing was decreased in storage of capsaicin-coated PE film, the flavor changes in slow.

Style APA, Harvard, Vancouver, ISO itp.

Sharma, Neha, Huong T. T. Phan, Tsuyoshi Yoda, Naofumi Shimokawa, Mun’delanji C. Vestergaard i Masahiro Takagi. "Effects of Capsaicin on Biomimetic Membranes". Biomimetics 4, nr 1 (13.02.2019): 17. http://dx.doi.org/10.3390/biomimetics4010017.

Pełny tekst źródła

Streszczenie:

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.

Style APA, Harvard, Vancouver, ISO itp.

Birsen, İlknur, V. Nimet İzgüt-Uysal, Hakan Soylu i İsmail Üstünel. "The effect of apelin-13 on gastric ischemia/reperfusion injury: the roles of sensory nerves and vagus nerve". Canadian Journal of Physiology and Pharmacology 98, nr 5 (maj 2020): 282–95. http://dx.doi.org/10.1139/cjpp-2019-0502.

Pełny tekst źródła

Streszczenie:

Apelin is a peptide that plays a role in physiological processes such as angiogenesis, apoptosis, and proliferation. The aim of this study was to investigate the role of capsaicin-sensitive afferent neurons and vagus in the effect of apelin against ischemia/reperfusion (I/R) injury. The experimental groups were (1) control, (2) I/R, (3) apelin + I/R, (4) vagotomy + I/R, (5) vagotomy + apelin + I/R, (6) capsaicin + I/R, (7) capsaicin + apelin + I/R, (8) lorglumide + I/R, and (9) lorglumide + apelin + I/R. To test the potential gastroprotective effect of apelin-13, apelin-13 (2 mg/kg i.v.) was administered just before both ischemia and reperfusion. A vagotomy was performed 1 week before I/R in the vagotomized groups; capsaicin (125 mg/kg s.c.) was administrated 2 weeks before I/R in the capsaicin-treated groups and lorglumide (5 mg/kg i.p.) was administered 30 min before I/R in the lorglumide-treated groups. After I/R, a variety parameters in gastric tissue were analyzed. cfos expression was determined in brainstem samples. In the I/R group, the lesion index, myeloperoxidase activity, lipid peroxidation, nitric oxide, and tumor necrosis factor-α increased, and mucosal blood flow, prostaglandin-E2, and calcitonin gene related peptide decreased. Apelin prevented the damaging effects of I/R and increased cfos expression in brainstem areas. Vagotomy, capsaicin, and lorglumide largely eliminated the gastroprotective effects of apelin-13. This study showed that sensory nerves and the vagus play regulatory roles in apelin-induced gastroprotection. Cholecystokinin may play a role in the effect of apelin through sensory neurons.

Style APA, Harvard, Vancouver, ISO itp.

Liu, L., W. Zhu, Z. S. Zhang, T. Yang, A. Grant, G. Oxford i S. A. Simon. "Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors". Journal of Neurophysiology 91, nr 4 (kwiecień 2004): 1482–91. http://dx.doi.org/10.1152/jn.00922.2003.

Pełny tekst źródła

Streszczenie:

Nicotine is an alkaloid that is used by large numbers of people. When taken into the body, it produces a myriad of physiological actions that occur primarily through the activation of neuronal nicotinic acetylcholine receptors (nAChRs). We have explored its ability to modulate TRPV1 receptors and voltage-gated sodium channels. The reason for investigating nicotine's effect on sodium channels is to obtain a better understanding of its anti-nociceptive properties. The reasons for investigating its effects on capsaicin-activated TRPV1 channels are to understand how it may modulate this channel that is involved in pain, inflammation, and gustatory physiology. Whole cell patch-clamp recordings from rat trigeminal ganglion (TG) nociceptors revealed that nicotine exhibited anesthetic properties by decreasing the number of evoked action potentials and by inhibiting tetrodotoxin-resistant sodium currents. This anesthetic property can be produced without the necessity of activating nAChRs. Nicotine also modulates TRPV1 receptors inducing a several-fold increase in capsaicin-activated currents in both TG neurons and in cells with heterologously expressed TRPV1 receptors. This sensitizing effect does not require the activation of nAChRs. Nicotine did not alter the threshold temperature (∼41°C) of heat-activated currents in TG neurons that were attributed to arise from the activation of TRPV1 receptors. In this regard, its effect on TRPV1 receptors differs from those of ethanol that has been shown to increase the capsaicin-activated current but decrease the threshold temperature. These studies document several new effects of nicotine on channels involved in nociception and indicate how they may impact physiological processes involving pain and gustation.

Style APA, Harvard, Vancouver, ISO itp.

Patwardhan, Chaitanya A., Eyad Alfa, Su Lu i Ahmed Chadli. "Progesterone Receptor Chaperone Complex–Based High-Throughput Screening Assay". Journal of Biomolecular Screening 20, nr 2 (2.09.2014): 223–29. http://dx.doi.org/10.1177/1087057114549147.

Pełny tekst źródła

Streszczenie:

Hsp90 and its co-chaperones are known to be important for cancer cell survival. The N-terminal inhibitors of Hsp90 that are in ongoing clinical trials as antitumor agents have unfortunately shown disappointing efficacies in the clinic. Thus, novel inhibitors of the Hsp90 machine with a different mechanism of action are urgently needed. We report here the development of a novel high-throughput screening assay platform to identify small-molecule inhibitors of Hsp90 and its co-chaperones. This assay quantitatively measures the ability of Hsp90 and its co-chaperones to refold/protect the progesterone receptor, a physiological client of Hsp90, in a 96-well plate format. We screened the National Institutes of Health clinical collection drug library and identified capsaicin as a hit molecule. Capsaicin is a Food and Drug Administration–approved drug for topical use in pain management. Cell survival assays showed that capsaicin selectively kills cancer cells and destabilizes several Hsp90 client proteins. Thus, our data may explain the seemingly pleotropic effect of capsaicin.

Style APA, Harvard, Vancouver, ISO itp.

Li, De-Pei, Shao-Rui Chen i Hui-Lin Pan. "VR1 Receptor Activation Induces Glutamate Release and Postsynaptic Firing in the Paraventricular Nucleus". Journal of Neurophysiology 92, nr 3 (wrzesień 2004): 1807–16. http://dx.doi.org/10.1152/jn.00171.2004.

Pełny tekst źródła

Streszczenie:

Neurons in the paraventricular nucleus (PVN) are important in regulating autonomic function through projections to the brain stem and spinal cord. Although the vanilloid receptors (VR1) are present in the PVN, their physiological function is scarcely known. In this study, we determined the role of VR1 receptors in the regulation of synaptic inputs and the excitability of spinally projecting PVN neurons. Whole cell patch-clamp recordings were performed on the PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Capsaicin significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) without changing the amplitude and decay time constant of mEPSCs. On the other hand, capsaicin had no effect on GABAergic miniature inhibitory postsynaptic currents (mIPSCs). The effect of capsaicin on mEPSCs was abolished by a specific VR1 antagonist, iodo-resiniferatoxin (iodo-RTX), or ruthenium red. Importantly, iodo-RTX per se significantly reduced the amplitude of evoked EPSCs and the frequency of mEPSCs. Removal of extracellular Ca2+, but not Cd2+ treatment, also eliminated the effect of capsaicin on mEPSCs. Furthermore, capsaicin caused a large increase in the firing rate of PVN neurons, and such an effect was abolished in the presence of ionotropic glutamate receptor antagonists. Additionally, the double-immunofluorescence labeling revealed that all of the VR1 immunoreactivity was colocalized with a presynaptic marker, synaptophysin, in the PVN. Thus this study provides the first evidence that activation of VR1 receptors excites preautonomic PVN neurons through selective potentiation of glutamatergic synaptic inputs. Presynaptic VR1 receptors and endogenous capsaicin-like substances in the PVN may represent a previously unidentified mechanism in hypothalamic regulation of the autonomic nervous system.

Style APA, Harvard, Vancouver, ISO itp.

Sugiura, Takeshi, Makoto Tominaga, Hirotada Katsuya i Kazue Mizumura. "Bradykinin Lowers the Threshold Temperature for Heat Activation of Vanilloid Receptor 1". Journal of Neurophysiology 88, nr 1 (1.07.2002): 544–48. http://dx.doi.org/10.1152/jn.2002.88.1.544.

Pełny tekst źródła

Streszczenie:

Bradykinin (BK) is an inflammatory mediator that plays a pivotal role in pain and hyperalgesia to heat in inflamed tissues by exciting nociceptors and sensitizing them to heat through activation of protein kinase C (PKC). It has been suggested that the capsaicin receptor (VR1), a nociceptor-specific cation channel sensitive to noxious heat, protons, and capsaicin, is a channel that is modified by BK in these effects. In this study, we examined how BK modulates the activity of VR1. We measured VR1 currents using the patch-clamp technique in human embryonic kidney-derived (HEK293) cells expressing VR1 and B2 BK receptor. We found that BK lowered the threshold temperature for activation of VR1 currents in HEK cells down to well below the physiological body temperature in a concentration-dependent manner through PKC activation. We also demonstrated that in capsaicin-sensitive dorsal root ganglion (DRG) neurons the activation threshold of heat-induced current, which is considered to be VR-1 mediated, was lowered by BK and that this effect was also mediated by PKC. These data further support the supposition that modulation of VR1 is a mechanism for the BK-induced excitation of nociceptors and their sensitization to heat.

Style APA, Harvard, Vancouver, ISO itp.

Kanazawa, H., H. Kamoi, T. Kawaguchi, S. Shoji, T. Fujii, S. Kudoh, K. Hirata i J. Yoshikawa. "PAMP is a novel inhibitor of the tachykinin release in the airway of guinea pigs". American Journal of Physiology-Lung Cellular and Molecular Physiology 272, nr 6 (1.06.1997): L1066—L1069. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1066.

Pełny tekst źródła

Streszczenie:

Proadrenomedullin NH2-terminal 20 peptide (PAMP), a newly identified hypotensive peptide, may play physiological roles in airway and cardiovascular controls. This study was designed to determine the mechanism responsible for the bronchoprotective effects of PAMP on capsaicin-induced bron-choconstriction in anesthetized guinea pigs. PAMP (10(-8)-10(-6) M) significantly inhibited capsaicin-induced bronchoconstriction in a dose-dependent manner. The bronchoprotective effect of PAMP (10(-6) M) was as large as that of isoproterenol (10(-7) M) and lasted > 10 min. The concentration of immunoreactive substance P (SP) in bronchoalveolar lavage fluid after administration of capsaicin (4 x 10(-6) M) was 120 +/- 10 fmol/ml. PAMP significantly inhibited the release of immunoreactive SP in a dose-dependent manner (60 +/- 6 fmol/ml for (10(-6) M PAMP, P < 0.01; 84 +/- 6 fmol/ml for 10(-7) M PAMP, P < 0.01; and 95 +/- 6 fmol/ml for 10(-8) M PAMP, P < 0.05). PAMP (10(-6) M) did not significantly affect exogenous neurokinin A (NKA) or NKA + SP-induced bronchoconstriction, whereas isoproterenol (10(-7) M) significantly inhibited exogenous tachykinin-induced bronchoconstriction. These findings suggest that the bronchoprotective effects of PAMP are mainly due to inhibition of the release of tachykinins at airway C-fiber endings.

Style APA, Harvard, Vancouver, ISO itp.

Raybould, H. E., i Y. Tache. "Cholecystokinin inhibits gastric motility and emptying via a capsaicin-sensitive vagal pathway in rats". American Journal of Physiology-Gastrointestinal and Liver Physiology 255, nr 2 (1.08.1988): G242—G246. http://dx.doi.org/10.1152/ajpgi.1988.255.2.g242.

Pełny tekst źródła

Streszczenie:

The pathway by which cholecystokinin octapeptide (CCK-8) inhibits motility of the proximal stomach and the role of this pathway in the CCK-induced delay in gastric emptying of a liquid meal has been studied in rats by selective destruction of vagal afferent C-fibers using bilateral perineural application of the sensory neurotoxin, capsaicin, 3 or 4 days prior to the experiment. The capsaicin treatment significantly attenuated the decrease in intragastric pressure in urethan-anesthetized rats in response to CCK-8 (0.1-100 pmol iv) compared with vehicle-treated controls. Removal of the celiac-superior mesenteric ganglion completely abolished the inhibitory action of CCK-8 on gastric motility in these rats. In contrast, only celiac ganglionectomy in combination with vagotomy abolished the CCK-8 effect in vehicle-treated controls. Intravenous injection of CCK-8 (300 pmol) 5 min before intragastric administration of a methylcellulose solution decreased gastric emptying by 55% in conscious control or vehicle-treated rats. Perivagal capsaicin treatment abolished the delay in gastric emptying induced by CCK-8. In addition, capsaicin treatment alone significantly increased gastric emptying. These results demonstrate that CCK-8 decreases gastric motility in the gastric corpus and delays gastric emptying by a capsaicin-sensitive vagal afferent pathway. These same afferent fibers may also play a physiological role in the gastric emptying of liquids.

Style APA, Harvard, Vancouver, ISO itp.

Lin, Qing, Jiri Palec̆ek, Veronika Palec̆ková, Yuan Bo Peng, Jing Wu, Minglei Cui i William D. Willis. "Nitric Oxide Mediates the Central Sensitization of Primate Spinothalamic Tract Neurons". Journal of Neurophysiology 81, nr 3 (1.03.1999): 1075–85. http://dx.doi.org/10.1152/jn.1999.81.3.1075.

Pełny tekst źródła

Streszczenie:

Nitric oxide mediates the central sensitization of primate spinothalamic tract neurons. Nitric oxide (NO) has been proposed to contribute to the development of hyperalgesia by activating the NO/guanosine 3′,5′-cyclic monophosphate (cGMP) signal transduction pathway in the spinal cord. We have examined the effects of NO on the responses of primate spinothalamic tract (STT) neurons to peripheral cutaneous stimuli and on the sensitization of STT cells following intradermal injection of capsaicin. The NO level within the spinal dorsal horn was increased by microdialysis of a NO donor, 3-morpholinosydnonimine (SIN-1). SIN-1 enhanced the responses of STT cells to both weak and strong mechanical stimulation of the skin. This effect was preferentially on deep wide dynamic range STT neurons. The responses of none of the neurons tested to noxious heat stimuli were significantly changed when SIN-1 was administered. Intradermal injection of capsaicin increased dramatically the content of NO metabolites, [Formula: see text] within the dorsal horn. This effect was attenuated by pretreatment of the spinal cord with a nitric oxide synthase (NOS) inhibitor, NG-nitro-l-arginine methyl ester (l-NAME). Sensitization of STT cells induced by intradermal injection of capsaicin was also prevented by pretreatment of the dorsal horn with the NOS inhibitors, l-NAME or 7-nitroindazole. Blockade of NOS did not significantly affect the responses of STT cells to peripheral stimulation in the absence of capsaicin injection. The data suggest that NO contributes to the development and maintenance of central sensitization of STT cells and the resultant mechanical hyperalgesia and allodynia after peripheral tissue damage or inflammation. NO seems to play little role in signaling peripheral stimuli under physiological conditions.

Style APA, Harvard, Vancouver, ISO itp.

Więcej źródeł

Rozprawy doktorskie na temat "Capsaicin Physiological effect"

Opheim, Maximilian Nicholas. "Effect of Capsaicin Supplementation on Performance of and Physiological Response to Repeated Sprinting". Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/41217.

Pełny tekst źródła

Streszczenie:

Aim: Fatigue during team sports requiring multiple sprints can result from the combined effects of metabolic, mechanical, neurological, and immune factors. The purpose of this study was to investigate the influence of capsaicin on performance of and the physiological response to an exercise test simulating the fitness demands of team sport game conditions. Methods: This study was a placebo-controlled, crossover design. Nineteen healthy male experienced athletes age 18-30 yr consumed either 3 g/d cayenne (25.8 mg/d capsaicin) or placebo for 1 wk. Directly following the supplementation period, they completed a repeated sprint test consisting of 15 30 m maximal effort sprints on 35 s intervals. Sprint times were recorded via electronic dual-beam timing system. Fasted blood draws for interleukin-6 (IL-6) were taken at baseline prior to supplementation, 45-min pretest, and immediately post test. Heart rate (HR), blood pressure (BP), rate of perceived exertion (RPE), muscle soreness (MS), and gastrointestinal distress (GD) were measured 1-min pretest, during, posttest, and 1-min posttest. MS was also measured for 3 d posttest. Results: Relative to the placebo, capsaicin significantly reduced maximum HR by 9.3%, total average HR by 8.5%, and sprinting average HR by 6.0% (P<0.05). Capsaicin caused GD of at least 2/5 in 24.5% of subjects. There was no difference between treatments in fastest or mean sprint time, fatigue, percent change or difference in IL-6, BP, RPE, sprint or posttest MS. Conclusion: Capsaicin did not influence repeated sprint performance or the inflammatory response, but reduced HR during intense activity and causes substantial GD.
Master of Science

Style APA, Harvard, Vancouver, ISO itp.

Helps, Stephen. "Cerebral blood flow in rats after treatment with the primary sensory neurotoxin capsaicin". Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09SM/09smh484.pdf.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Helps, Stephen. "Cerebral blood flow in rats after treatment with the primary sensory neurotoxin capsaicin". Thesis, 1987. http://hdl.handle.net/2440/110498.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Książki na temat "Capsaicin Physiological effect"

Muhammed, Majeed, red. Capsaicin: The anti-arthritic phytochemical. Piscataway, NJ: Nutriscience Publishers, 1997.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Daniell, Grace. The functional role of capsaicin-sensitive baro- and chemo-afferents. 1990.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Mozsik, Gyula, Andras Debreceni i Kazuichi Okazaki. The Capsaicin- And Helicobacter Strains-Induced Cellular Mechanisms of the Gastric Mucosa in Animals and Humans. Akademiai Kiado, 2001.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

South, Elizabeth H. Depletion of substance P immunoreactivity and alterations in cholecystokinin-induced reduction of food intake following capsaicin treatment. 1986.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

N, Wood John, red. Capsaicin in the study of pain. London: Academic Press, 1993.

Znajdź pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Oferujemy zniżki na wszystkie plany premium dla autorów, których prace zostały uwzględnione w tematycznych zestawieniach literatury. Skontaktuj się z nami, aby uzyskać unikalny kod promocyjny!