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Blood Circulation Stimulation Properties of Cayenne Pepper:A Review

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Abstract

Cayenne pepper (also called Capsicum frutescence) is a stimulating herb made from the dried pods of chili peppers and is well known for its pungent taste and smell. Cayenne is a popular spice used in many different regional styles of cooking, but it has also been used medicinally for thousands of years. Cayenne is often referred to as chili, which is the Aztec name for cayenne pepper. The main medicinal properties of cayenne are derived from a chemical called capsaicin. Capsaicin is the ingredient which gives peppers their HEAT. A pepper's capsaicin content ranges from 0-1.5%. Peppers are measured according to heat units. The degree of heat determines the peppers' usage and value. Generally, the hotter the pepper, the more capsaicin it contains. In addition to adding heat to the pepper, capsaicin acts to reduce platelet stickiness and relieve pain. Other constituents of cayenne are vitamins E, vitamin C and carotenoids. Today cayenne is used worldwide to treat a variety of health conditions, including poor Circulation, weak digestion, heart disease, chronic pain, sore throats, headache sand toothache Cayenne is the greatest herbal aid to circulation and can be used on a regular basis. Dr. Richard Schulze, the medical herbalist, says that "If you master only one herb in your life, master Cayenne pepper. It is more powerful than any other
IOSR Journal of Applied Chemistry (IOSR-JAC)
e-ISSN: 2278-5736.Volume 11, Issue 5 Ver. I (May. 2018), PP 78-83
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DOI: 10.9790/5736-1105015743 www.iosrjournals.org 78|Page
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
MukulChauhan, Chhavi Kant, ChitraNegi And PrachiChauhanDepartment of chemistry,
School of Applied Science ShriVenkateshwara University, Gajraula, U.P. , IndiaCorresponding
Author:MukulChauhan, Chhavikant
Abstract: Cayenne pepper (also called Capsicum frutescence) is a stimulating herb made from the dried pods of
chili peppers and is well known for its pungent taste and smell. Cayenne is a popular spice used in many different
regional styles of cooking, but it has also been used medicinally for thousands of years. Cayenne is often referred to
as chili, which is the Aztec name for cayenne pepper. The main medicinal properties of cayenne are derived from a
chemical called capsaicin. Capsaicin is the
ingredient which gives peppers their HEAT. A pepper's capsaicin content ranges from 0-1.5%. Peppers are
measured according to heat units. The degree of heat determines the peppers' usage and value. Generally, the hotter
the pepper, the more capsaicin it contains. In addition to adding heat to the pepper, capsaicin acts to reduce platelet
stickiness and relieve pain. Other constituents of cayenne are vitamins E, vitamin C and carotenoids. Today cayenne
is used worldwide to treat a variety of health conditions, including poor Circulation, weak digestion, heart disease,
chronic pain, sore throats, headache sand toothache Cayenne is the greatest herbal aid to circulation and can be
used on a regular basis. Dr. Richard Schulze, the medical herbalist, says that "If you master only one herb in your
life, master Cayenne pepper. It is more powerful than any other."
Date of Submission:15-05-2018 Date of acceptance:21-05-2018
Introduction
Cayenne pepper belongs to the capsicum family, and its botanical name is capsicumannuum. It is the red chili
pepperthat is used to add flavor in food and has high medicinal values.Cayenne contains vitamin E, vitamin C,
vitamin K, carotenoids, and the complete B complex vitamins. It is also a source of organic calcium, potassium,
manganese, and dietary fiber.For health and medicinal purposes, you only need to drink small amounts of cayenne
powder, mixed in a glass of water.[1-2]
Risk factors for cardiovascular disease (CVD) include metabolic and vascular factors, such as hypercholesterolemia,
hyperglycaemia, hyperinsulinemia, obesity, hypertension and arterial stiffness. One approach to reducing CVD risk
is to reduce body weight. Obesity elevates the risk of hyperglycaemia, hyperinsulinemia, and vascular resistance
(Eckel et al., 2005; Moller and Kaufman, 2005; Sundell, 2005). Decreasing energy input and increasing energy
output (e.g., low energy diets and increasing exercise) are the two approaches for weight reduction. Chilli or its
active component capsaicin has been shown to increase energy expenditure and/or fat oxidation (in animals and
humans) and lower serum lipids (in animals).[3-5]
How cayenne pepper can helps us
Cayenne pepper increases blood circulation. It also draws the blood to where it is especially needed.
Because of these special abilities, it can be used to help you in many ways. Cayenne is a counterirritant; it brings
blood to the surface and allows the toxins to be taken away. It wonderfully improves blood circulation[.7]
The benefits of cayenne are almost too unbelievable; but its reputation keeps growing and growing, and deservedly
so. It can do everything from killing cancer cells in the prostate, lungs, and pancreas to immediately stopping a heart
attack within 30 seconds. Incredible, but successful in many instances. The health benefits of cayenne pepper
include improvements in regard to digestion, immunity, heart diseases, dyspepsia, inflammation, headache, throat
congestion, and blood circulation. Cayenne pepper improves the effectiveness of other herbs.[8-11]
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 79|Page
Prevents heart attack
There are evidences that prove that giving cayenne extract orally, to a patient, helps to stop heart attack.
Cayenne helps to reduce cholesterol levels in the blood. Cayenne helps to dissolve fibrin, which causes formation of
blood clots. It also reduces triglyceride levels. It is excellent for any type of internal hemorrhage.Cayenne pepper
increases metabolism by immediately speeding up the flow of blood in the arteries and veins.[15-16].
This herb is a great food for the circulatory system. It feeds the necessary elements into the cell structure of
the arteries, veins, and capillaries; so that these regain the elasticity of youth again, and the blood pressure adjusts
itself to normal.
It improves blood circulation. When any body part is sick, the blood flow to that area is usually affected. Cayenne
helps to remove entire blood congestion, stimulates the blood flow, makes sure that the vitamins are properly
delivered to all areas, and waste is removed.[13-14]
Dr. John Christopher, the famed natural herbalist, was relentlessly harassed by the government for his practice of
herbal medicine, all the while assisting patients in curing heart disease, cancer, tuberculosis, infertility, rheumatism,
leukemia, and many other conditions with herbs. He could instantly stop a heart attack if he could get the patient to
drink a glass of warm cayenne water. He said, “A teaspoon of cayenne should bring the patient out of the heart
attack.” For internal hemorrhaging (bleeding inside the body), if the patient can drink a glass of extra warm cayenne
water, Dr. Christopher wrote, “by the count of ten the bleeding will stop. Instead of all the pressure being
centralized, it is equalized and the clotting
becomes more rapid.” With over 700,000 Americans experiencing a stroke each year and almost half a million dying
yearly of either heart disease or related issues, cayenne pepper is worth keeping on your shelf. Capsicum may be
valuable in the prevention and treatment of blood clots. Cayenne is also great for heartburn.[19-22]
Healing the sick part of body
When you have a sick area, there ‘soften a restriction of blood flow to that area. Blood flow is what takes
nutrition and the healing properties of herbs to those cells. Blood flow is also what Carries out and removes waste
material. Cayenne pepper is like TNT. It blasts through all that blockage to get to that area which is sick, taking with
it all the minerals and vitamins from the Foods you eat, and all the vital chemicals from the herbs you take-all the
way to the sick area.
Cayenne pepper is usually labeled 40,000, 60,000, 90,000 or more heat units. Generally, the higher the number of
heat units, the more beneficial. The lower-heat cayenne peppers are a lot less efficient, and they are the ones which
are most highly contaminated. These are the ones you see labeled for 30,000 heat units. These are the ones to stay
away from.[25-27]
Use of cyanne powder in place of capsule
It is recommended that the cayenne powder be used, as opposed to capsules. It is believed that you are only
getting a small part of the potential effect of cayenne pepper by taking it in capsules. When you put cayenne in your
mouth, your stomach secretes digestive juices before the cayenne ever gets there. So when the cayenne gets down
there, your stomach is ready for it.
But if you swallow a capsule, your tongue tastes nothing. A capsule goes down in your stomach, and your stomach
notices nothing, at first. Then, 5minutes later the gelatin bursts, and you have a ½ tea spoon of cayenne pepper in
your stomach and your body is shocked. You surprised it. What is going on is that some of cayenne's healing action
occurs right in your mouth. As cayenne touches your tongue, the cayenne absorbs in seconds and nerve endings send
signals throughout the body-sending waves of fresh blood throughout your body.[32-37]
Controlls high blood pressure and regulates the temperature of body
Cayenne pepper for high blood pressure is certainly one of its core uses; but cayenne cleans the arteries as
well, helping to rid the body of the bad LDL cholesterol and triglycerides. It is an excellent home treatment for mild
high blood pressure and high blood cholesterol levels. [42]
Cayenne preparations prevent platelets from clumping together and accumulating in the blood, allowing the blood to
flow more easily. Since it is thought to help improve circulation, it’s often used by those who have cold hands and
feet. It equalizes the blood circulation in the arterial and venous system, and produces natural warmth in your body.
It does this by regulating the flow of blood from the head to the feet, so that the pressure is equalized. It
influencesthe heart immediately; then it gradually extends its effects to the arteries, capillaries, and nerves.[39-41]
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 82|Page
Avoid use of cayenne in case of
Keep in mind that regularly taking large amounts of cayenne may eventually damage the kidneysand
lead to pleurisy and other conditions caused by weakened kidney function. It is the kidneys which have to process
the cayenne by extracting it from the blood into the urine. Too much cayenne, too frequently, weakens kidney
function. If you’ve ever accidentally rubbed your eyes after cutting hot peppers, you know this herb should be
handled carefully. Cayenne pills may cause a burning sensation in the throat, stomach, or rectum of sensitive
individuals. Some people may tolerate cayenne fluid preparations or combination products better than tablets or
capsules. Others may find cayenne pepper in the diet easier to digest than cayenne medications. Only use small,
cautious doses. Avoid getting cayenne into the eyes or open wounds. Do not use topical applications of cayenne
products too frequently; since there is some concern that nerve damage could occur with daily repetitive use.
Cayenne placed directly on the skin can cause burns and even blisters; so dilute a cayenne preparation in oil before
placing it on the skin. Or mix it with flour and water until it forms a paste, which you can spread on muslin, to
prepare a poultice. You also can mix cayenne with orrisroot powder and dust it very lightly on heavily oiled skin,
working it in with massage.[45-49]
Do not use cayenne in cases of high fever (104 degrees Fahrenheit or above). Cayenne preparations are not
recommended for use by individuals who have rapid heart rates or who become overheated or perspire easily. Avoid
internal use of cayenne in cases of asthma and gastrointestinal irritation or inflammation, except under the
supervision of an experienced herbalist. Do not use cayenne on broken skin. Like all other foods or herbs, we have
to also be careful when using this herb. Excessive consumption may cause burning sensations in the throat, stomach,
or rectum. When cooking or making medicines with cayenne peppers, you must take into account the widely varying
intensities (heat) of different peppersfrom very mild to extremely fiery.[50-51]
Cancer and detoxification
Cayenne pepper is also very well known for its cancer fighting properties. It may prevent the spread of
cancerous cells, while initiating apoptosis or programmed cell death. In lab studies, cayenne was able to kill
prostate, breast, stomach, pancreas and lung cancer. [17-19]
However, the question is, would it work on us?
Due to benefits of cayenne pepper, herb is also used in detoxification formulas since it exhibits anti- bacterial, anti-
viral and anti- fungal properties. Capsaicin from cayenne is very well absorbed from the digestive track into the
blood stream. On the other hand, it is questionable how much should we consume, in order to experience cayenne
benefits and avoid the side effects.[53-55]
Side effects
Possible side effects include nausea, vomiting, stomachaches and diarrhea. When applied to the skin and
left for some time, the herb will provoke burning reaction. This is especially dangerous, if cayenne comes in contact
with eyes. Higher doses of cayenne may lead to kidney and liver damage, severe gastrointestinal problems
And even death. Besides capsaicin, the herb contains other flavonoids, too, which may be Carcinogenic in high
amounts.[21-24]
Structure
[28]
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 82|Page
Chemical composition
VITAMINS AND MINERALS:
OTHERS:
Ca .26%
albumen 2.4%
p .09
pectin 2.33
K .17
gums 1.3
Na tr
starch 2.0
CI tr
capsaicin .43
Mg .31
capsacutin oil 16.35
Fe .0006
pentosans totaling 8.59 solaine
Mntr
xanthenes .82
Cu tr
oleic acid
Zn tr
palmitic acid 1.85
Carotene-various carotenoid pigment.
no carotene
steanc acid
A 12,137 Mg/Ib
fatty acids
B-1 78
B-2 12
C (ascorbic acid) 493
[23-24]
Conclusion
Cayenne is cheap and easily available herb found in supermarkets. You can use it to destroy blood clots, improve
lipid profiles, heart function and above all, circulation. However, it is also used for treating viral infections such as
shingles and herpes, arthritis, diabetes, muscle pain, as well as for relieving pain associated with gum disease and
headaches. For which ever reason you decide to get you some benefits of cayenne pepper, don't go overboard. Too
much capsaicin can be counterproductive.
Reference
1. Zsombok A. Vanilloid receptorsrole of capsicum family in whole body metabolism?Evidence from TRPV1. J Diabetes Complications
2013;27:28792. 2. Nilius B,
Szallasi A. CVD targets metabolism: from the science of basic research to the art of medicine.Pharmacol Rev2014;66:676814.3. Zhu Z, Luo Z,
Ma S, et al. TRP channels and their implications in metabolic diseases and blood circulation. Pflugers Arch2011;461:21123.4. Iida T, Moriyama
T, Kubota K, et al. TRPV1 activation and induction of nociceptive response by a non-pungent capsaicin-like compound, capsiate.
Neuropharmacology2003;44:95867. 5. Kawada T, Suzuki T, Takahashi M, et al. Gastrointestinal absorption and metabolism of capsaicin and
affected metabolism in rats. ToxicolApplPharmacol1984;72:44956. 6. Rollyson WD,
Stover CA, Brown KC, et al. Bioavailability of capsaicin and its implications for drug delivery. J Control Release 2014;196:96105.7. Chaiyasit K,
Khovidhunkit W, Wittayalertpanya S. Pharmacokinetic and the effect of capsaicin in Capsicum frutescens on decreasing plasma glucose level. J
Med Assoc Thai 2009;92:10813. 8. Kopanitsa MV,
Panchenko VA, Magura EI, et al. Capsaicin blocks Ca2+channels in isolated rat trigeminal and hippocampal neurones. Neuroreport1995;6:2338
40. 9. Sim JH, Kim YC, Kim SJ, et al.
Capsaicin inhibits the voltage-operated calcium channels intracellularly in the antral circular myocytes of guinea-pig stomach. Life
Sci2001;68:234760. 10. Vyklicky L, Novakova-Tousova K, Benedikt J, et al. 10.Calcium-dependent desensitization of
vanilloid receptor TRPV1:a mechanism possibly involved in analgesia induced by topical application of capsaicin. Physiol Res 2008;57(Suppl
3):S5968. 11. Kissin I. Vanilloid-induced conduction analgesia:
selective, dose-dependent, long-lasting, with a low level of potential neurotoxicity. AnestAnalg2008;107:27
12. Knotkova H, Pappagallo M, Szallasi A. Capsaicin (TRPV1 Agonist) therapy for pain relief: farewell or revival? Clin J Pain 2008;24:14254.
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 82|Page
13. Jones VM, Moore KA, Peterson DM. Capsaicin 8% topical patch (Qutenza)a review of the evidence. J Pain Palliat Care
Pharmacother2011;25:3241.
14. Gunthorpe MJ, Szallasi A. Peripheral TRPV1 receptors as targets for drug development: new molecules and mechanisms.Curr
Pharm Des 2008;14:3241.
15. Czikora A, Rutkai I, Pasztor ET, et al. Different desensitization patterns for sensory and vascular TRPV1 populations in the rat:
expression, localization and functional consequences. PLoS ONE 2013;8:e78184.
16. Fleming I, Busse R. Signal transduction of eNOS activation.Cardiovasc Res1999;43:53241.
17. Chen Z, Peng IC, Cui X, et al. Shear stress, SIRT1, and effect on cancer cells. ProcNatlAcadSci U S A2010;107:1026873. 18. Young
A, Wu W, Sun W, et al. Flow activation of AMP-activated protein kinase in vascular endothelium leads to Kruppel-like factor 2 expression.
ArteriosclerThrombVascBiol2009;29:19028. 19. Wang W, Ha CH,
Jhun BS, et al. Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS.
Blood2010;115:29719. 20. Parmar KM,
Larman HB, Dai G, et al. Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2. J Clin Invest 2006;116:4958.
21. SenBanerjee S, Lin Z, Atkins
GB, et al. KLF2 Is a novel transcriptional regulator of nausea,stomachacheeproinflammatory activation. J Exp Med2004;199:130515.
22. Lin Z, Kumar A, SenBanerjee S, et al. Kruppel-like
factor 2 (KLF2) regulates endothelial thrombotic function. Circ Res2005;96:e4857.23. Fledderus JO, van Thienen JV, Boon RA, et al. Prolonged
shear stress and KLF2 suppress constitutive proinflammatory chemical composition through inhibition of ATF2. Blood2007;109:424957.
24. Fledderus JO, Boon RA, Volger OL, et al. KLF2 flavanoids the
antioxidant transcription factor Nrf2 for activation in endothelial cells. ArteriosclerThrombVascBiol2008;28:133946.
25. Lo YC, Hsiao HC, Wu DC, et al. A novel capsaicin derivative VOA induced relaxation
and regulation of body temp. in rat mesenteric and aortic arteries: involvement of CGRP, NO, cGMP, and endothelium-dependent activities.
CardiovascPharmacol2003;42:51120. 26. Ching LC, Kou YR, Shyue SK, et al. Molecular mechanisms of activation of endothelial nitric
oxide synthase mediated by transient receptor potential vanilloid type 1. Cardiovasc Res2011;91:492501.
27. Yang D, Luo Z, Ma S, et al. Activation of TRPV1 by dietary capsaicin improves endothelium-dependent
vasorelaxation and prevents hypertension. Cell Metab 2010;12:13041.
28. Xu X, Wang P, Zhao Z, et al. Activation of capsasin and its structurepotential vanilloid 1 by dietary capsaicin delays the
onset of stroke in stroke-prone spontaneously hypertensive rats. Stroke 2011;42:324551.
29. Ma L, Zhong J, Zhao Z, et al. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis. Cardiovasc
Res 2011;92:50413. 30. Zhao
JF, Ching LC, Kou YR, et al. Activation of TRPV1 prevents OxLDL-induced lipid CardiovascPharmacol accumulation and TNF-alpha-induced
inflammation in macrophages: role of liver X receptor alpha. Mediators Inflamm2013;2013:925171.31. Fragasso G, Palloshi A, Piatti PM, et al.
Nitric-oxide mediated effects of transdermal capsaicin patches on the ischemic threshold in patientswith stable coronary disease. J
2004;44:3407. 32. Hao X, Chen J, Luo Z, et al. TRPV1
activation prevents high-salt diet-induced nocturnal hypertension in mice. Pflugers Arch 2011;461:34553.33. Li L, Wang F, Wei X, et al.
Transient receptor potential vanilloid 1 activation by dietary capsaicin promotes urinary sodium excretion by inhibiting cayenne pepper
epithelial sodium channel alpha subunit-mediated sodium reabsorption. Hypertension 2014;64:397404.34. Bratz IN, Dick GM, Tune JD, et al.
Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome. Am J Physiol Heart CircPhysiol
2008;294:H248996. 35. Zygmunt PM, Petersson J, Andersson
DA, et al. Vanilloid receptors on sensory nerves mediate the vasodilator action of anandamide. Nature 1999;400:4527.
36. Czikora A, Lizanecz E, Bako P, et al. Structure-
activity relationships of vanilloid receptor agonists for arteriolar TRPV1. Br J Pharmacol 2012;165:180112.
37. Patane S, Marte F, La Rosa FC, et al. Capsaicin and arterial
hypertensive crisis. Int J Cardiol2010;144:e267. 38. Dutta A, Deshpande SB. Mechanisms underlying the
hypertensive response induced by capsaicin. IntJ Cardiol2010;145:3589. 39. Sun J, Pu Y, Wang P, et al. TRPV1-mediated UCP2 upregulation
ameliorates hyperglycemia-induced endothelial dysfunction. CardiovascDiabetol2013;12:69.
40. Li L, Chen J, Ni Y, et al. TRPV1 activation prevents nonalcoholic fatty liver
through UCP2 upregulation in mice. Pflugers Arch 2012;463:72732.
41. Gao F, Liang Y, Wang X, et al. TRPV1 activation attenuates high-salt diet-induced
cardiac hypertrophy and fibrosis through PPAR-delta upregulation. PPAR Res 2014;2014:491963
42. Planavila A, Rodriguez-Calvo R, Jove M, et al. Peroxisome proliferator-activated receptor and regulation of body temperature beta/delta
activation inhibits hypertrophy in neonatal rat cardiomyocytes. Platelets clumping and accumulation.2005;65:83241. 43. Negre-
Salvayre A, Hirtz C, Carrera G, et al.A role for uncoupling protein-2 as a regulator of mitochondrial hydrogen peroxide generation.FASEB J
1997;11:80915.
44.Echtay KS, Roussel D, St-Pierre J, et al. Superoxide activates mitochondrial uncoupling proteins. Nature2002;415:969. 45. Echtay KS, Brand
MD. 4-hydroxy-2-nonenal and uncoupling proteins damaging kidney: an approach for regulation of mitochondrial ROS production. Redox Rep
2007;12:269. 46. Piconi L, Quagliaro L,
Assaloni R, et al. Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction.
Diabetes Metab Res Rev 2006;22:198203.
47. Nishikawa T, Kukidome D, Sonoda K, et al. Impact of preparation and combination product on mitochondrial ROS production on diabetic
vascular complications. Diabetes Res ClinPract 2007;77(Suppl 1):S415s
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 83|Page
48 .Tian XY, Wong WT, Xu A, et al. Uncoupling protein-2 protects endothelial function in incrasingheart beat. Circ Res 2012;110:121116.49.
Cheurfa N, Dubois-Laforgue D, Ferrarezi DA, et al. The common -866G>A variant in the promoter of UCP2 is associated with decreased risk of
coronary artery disease in type 2 diabetic men. Diabetes2008;57:10638. 50.
Serviddio G, Sastre J, Bellanti F, et al. Mitochondrial involvement in non-alcoholic steatohepatitis.Mol Aspects Med 2008;29:2235.51. Serviddio
G, Bellanti F, Tamborra R, et al. Uncoupling protein-2 (UCP2) induces mitochondrial proton leak and increases susceptibility of non-alcoholic
steatohepatitis (NASH) liver to ischaemia-reperfusion injury. Gut2008;57:95765. 52. Li Q, Li L, Wang F,
et al. Dietary capsaicin prevents nonalcoholic fatty liver disease through transient receptor potential vanilloid 1-mediated peroxisome
proliferator-activated receptor delta activation. Pflugers Arch 2013;465:130316. 53. McCarty MF. High
mitochondrial redox potential may promote cancer detoxification induction and activation of UCP2 in hepatocytes during hepatothermic
therapy. Med Hypotheses 2005;64:121619. 54. Kang JH, Kim CS,
Han IS, et al. Capsaicin, a spicy component of hot peppers, modulates adipokine gene expression and protein release from obese-mouse
adipose tissues and isolated adipocytes, and suppresses the inflammatory responses of adipose tissue macrophages. FEBS Lett 2007;581:4389
96. 55. Kang JH, Tsuyoshi
G, Le NH, et al. Dietary capsaicin attenuates metabolic role in cancer detoxification genetically obese diabetic mice. J Med Food2011;14:310
15.
MukulChauhan, Chhavi Kant "Blood Circulation Stimulation Properties of Cayenne Pepper:A
Review." IOSR Journal of Applied Chemistry (IOSR-JAC) 18.5(2018): 01-06.
IOSR Journal of Applied Chemistry (IOSR-JAC) is UGC approved Journal with Sl. No. 4152,
Journal no. 46132.
... The pepper's high nutritional value results in high year-round demand on the market. Pepper fruits are used as a dried powder in salads, pickles, filling, sauces, and sauce (Mukul et al.,2018;Toyer, 2021). ...
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We investigated the molecular mechanism underlying the role of transient receptor potential vanilloid type 1 (TRPV1), a Ca(2+)-permeable non-selective cation channel, in the activation of endothelial nitric oxide (NO) synthase (eNOS) in endothelial cells (ECs) and mice. In ECs, TRPV1 ligands (evodiamine or capsaicin) promoted NO production, eNOS phosphorylation, and the formation of a TRPV1-eNOS complex, which were all abrogated by the TRPV1 antagonist capsazepine. TRPV1 ligands promoted the phosphorylation of Akt, calmodulin-dependent protein kinase II (CaMKII) and TRPV1, and increased the formation of a TRPV1-Akt-CaMKII complex. Removal of extracellular Ca(2+) abolished the ligand-induced increase in the phosphorylation of Akt and CaMKII, formation of a TRPV1-eNOS complex, and eNOS activation. Inhibition of PI3K and CaMKII suppressed the ligand-induced increase in TRPV1 phosphorylation, formation of a TRPV1-eNOS complex, and eNOS activation. TRPV1 activation increased the phosphorylation of Akt, CaMKII, and eNOS in the aortas of wild-type mice but failed to activate eNOS in TRPV1-deficient aortas. Additionally, TRPV1 ligand-induced angiogenesis was diminished in eNOS- or TRPV1-deficient mice. When compared with apolipoprotein E (ApoE)-deficient mice, ApoE/TRPV1-double-knockout mice displayed reduced phosphorylation of eNOS, Akt, and CaMKII in aortas but worsened atherosclerotic lesions. TRPV1 activation in ECs may trigger Ca(2+)-dependent PI3K/Akt/CaMKII signalling, which leads to enhanced phosphorylation of TRPV1, increased TRPV1-eNOS complex formation, eNOS activation and, ultimately, NO production.
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