Friday, February 14, 2020

Herbal Artichoke Protects the Blood Vessels Against the Risk of CVD

Vasoprotection is a term characterized by protecting your blood vessel against the onset of heart disease and stroke.

Blood vessel formed part of the vascular or circulation system that transports the oxygen and nutrients blood to the body tissue and removes unnecessary waste products.

The circulation system also plays an essential role in transporting hormones to the body's needs.

The most common cause of abnormal vascular system is the accumulation of plaque on the arterial wall due to the deposit blood cholesterol and other substances such as calcium and cadmium, leading to hardening and narrowing the arteries over time.

Atherosclerosis is a disease associated with plaque that builds up inside the arteries, a major cause of heart disease and stroke.

Vascular disease can be serious. Blood clots can clog vessels and block blood flow to the heart or brain.


Some researchers suggested that widespread vascular disease in the Western world probably is associated with the promotion of the Western diet over the past few decades.

Dr. Rachel P Ogilvie, the lead scientist, in the examination of the Western diet in the risk of vascular disease, wrote, "Peripheral arterial disease (PAD) is a costly source of morbidity and mortality among older persons in the United States. Dietary intake plays a role in the development of atherosclerotic cardiovascular disease".


And, "...greater meat consumption was associated with a higher risk".

Artichoke is a perennial thistle of Cynara cardunculus species of the Cynara genus, belonging to the family Carduoideae native to Southern Europe around the Mediterranean.



The herbal plant has been used in traditional medicine as liver protective and detoxified agents, and to treat digestive disorders, abdominal pain gas and bloating, etc.

Researcher on the finding a natural therapeutic with vasoprotective activity investigated investigate the effects of artichoke on iNOS expression in human coronary artery smooth muscle cells (HCASMC).

The study included HCASMC incubated with a cytokine mixture to induce nitric oxide synthases (iNOS) mRNA expression.

Application of an artichoke leaf extract (1-100 µg/mL, 6 h or 24 h) inhibited the levels of iNOS in concentration- and time-dependent manner.

By inhibiting the expression of iNOS, the artichoke leaf extract also reduced pro-inflammatory cytokine activation by iNOS.


Where nitric oxide synthases are a family of enzymes involved in the production of nitric oxide from L-arginine.

And, Nitric oxide (NO) induces an anti-inflammatory effect under normal physiological conditions. However, under abnormal conditions, NO is considered a pro-inflammatory mediator-induced inflammation.

Additional analysis of the extract against NO in the induction of vascular inflammation and intimal hyperplasia, researchers found that the vasoprotection of the extract was attributed to the four well-known artichoke compounds including cynarin, cyanidin, luteolin, and cynaroside.


In other words, artichoke contains both endothelial nitric-oxide synthase (eNOS-exhibition and iNOS-inhibition compounds.

Where eNOS- is a critical regulator of cardiovascular homeostasis.

Furthermore, in order to reveal more information about nitric oxide (NO) produced by endothelial nitric-oxide synthase (eNOS) represents an antithrombotic and anti-atherosclerotic principle in the vasculature, researchers examined the effect of artichoke extract incubated with human umbilical vein endothelial cells (HUVECs),

According to the luciferase reporter gene assay, artichoke leaf extract (ALE) increased the activity of the human eNOS promoter in EA.hy 926 cells, a cell line derived from human umbilical vein endothelial cells (HUVECs).

By comparing the application of different doses used in the experiment, researchers found organic subfraction from ALE was more potent in this respect than the crude extract, whereas an aqueous subfraction of ALE was without effect in EA.hy 926 cells.


Furthermore, injection of ALE and the organic subfraction increased eNOS mRNA expression and eNOS protein expression both in EA.hy 926 cells and HUVECs.

Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, compared to no effect of caffeoylquinic acids cynarin and chlorogenic acid.

In other words, artichoke increased eNOS gene transcription for the protection of cardiovascular profile was also attributed additionally by the lipid-lowering and antioxidant properties.

Taken altogether, artichoke may be considered a functional remedy for the protection of blood vessels against the risk of cardiovascular disease with no side effects, pending to the validation of larger sample size and multicenter human study.

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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.

References
(1) Artichoke, cynarin and cyanidin downregulate the expression of inducible nitric oxide synthase in human coronary smooth muscle cells by Xia N1, Pautz A1, Wollscheid U1, Reifenberg G1, Förstermann U1, Li H. (PubMed)
(2) Flavonoids from artichoke (Cynara scolymus L.) up-regulate endothelial-type nitric-oxide synthase gene expression in human endothelial cells by Li H1, Xia N, Brausch I, Yao Y, Förstermann U. (PubMed)
(3) Dietary intake and peripheral arterial disease incidence in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study by Rachel P Ogilvie, Pamela L Lutsey, Gerardo Heiss Aaron R Folsom, and Lyn M Steffen (Oxford)

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