The Bioacive Compound Which Might Cure Atherosclerosis, According to Studies

By Kyle J. Norton

Sinigrin may be used as a bioactive ingredient for the prevention and treatment of atherosclerosis, according to studies.

Atherosclerosis is a medical condition caused by plaques accumulated on the wall of the arteries, leading to narrowing the arteries in transporting oxygenated blood to the heart and other parts of the body.

Depending on the blood obstruction, atherosclerosis can induce different types of heart disease and stroke.

Plaque is the make of cholesterols, calcium, and other toxic substances, including cadmium.

According to the statistics provided by Atherosclerosis Open Acess, 32% of deaths account for atherosclerosis. 13.8% prevalence is among adults of 20 years and above. In 2010, coronary heart disease mortality rate was about 60%.

Risk factors of atherosclerosis include high blood pressure and cholesterol, diabetes,  being overweight or obese, unhealthy diet,  family history of heart disease and physical inactivity, particularly smoking.

Some researchers suggested that since cholesterol make up a big part in the plaque, an unhealthy diet with a high saturated trans fat, red meat and processed meat may be the major cause of atherosclerosis.

In other words, the Western diet is one of the major culprits that cause the majority of cases of atherosclerosis. 

Dr. Meifang Wang, the lead researcher in the study of “Western Diet Increases Inflammatory Responses and Atherosclerosis Progression via IGF-1 Receptor in ApoE-Deficient Mice” said, “….lowered circulating IGF-1 increases atherosclerosis progression in atherosclerosis-prone apolipoprotein E-deficient mice (ApoE−/−) while increased circulating IGF-1 downregulates vascular pro-inflammatory cytokine gene expression, reduces systemic and vascular oxidant stress, vascular cytokine expression, and decreases atherosclerosis progression”.

And, “the pro-inflammatory phenotype that is enhanced by WD in ApoE−/− mice is further enhanced by specific IGF1R deficiency in monocytes/macrophages, and may consequently increase atherosclerosis progression”.

The results suggested that the Western diet-induced atherosclerosis progression through the increase of production of pro-inflammatory cytokines and decrease of the function of insulin-like growth factor-1 (IGF-1) as a mediator of anabolic responses in many cells and tissues.

Sinigrin is a phytochemical glucosinolate, belonging to the family of glucosides found abundantly in Brussels sprouts, broccoli, the seeds of black mustard, etc.

Scientists on finding a natural bioactive compound for the treatment of atherosclerosis examined the effect of sinigrin against plaque accumulation on the arterial walls.

On atherosclerosis in ApoE-/- mice, injection sinigrin exerted a significant effect in the inhibition of the serum concentrations of lactate dehydrogenase (LDH), triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), calcium (Ca2+), and pro-inflammatory cytokines associated with plaque accumulated on the wall of the arteries.

Furthermore, oral administration of sinigrin attenuated the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), which form a part of immunoglobulin superfamily in inflammatory and immune responses. 

Moreover, injection also reduced the expression of genes C-C motif chemokine ligand 2 (CCL2), and CCL5 on aorta tissues associated with the risk of atherosclerosis.

The expression of low-density lipoprotein was also reduced by the injection of sinigrin observed by some keys regulators of cholesterol such as sterol regulatory element-binding protein-2 (SREBP-2).

Interestingly, increased the concentration of sinigrin at the dose up to 100 μg/ml also significantly suppressed the levels of Tumor necrosis factor (TNF-α) and nuclear translocation of NF-κB, cell signaling protein (cytokine) involved in systemic inflammation.

Additionally, at a contraction ut to 100 μg/ml, sinigrin inhibited the c-Jun-NH (2)-terminal kinase (JNK) signaling pathway which plays a critical role in regulating cellular differentiation.

The findings strongly suggested that sinigrin inhibited the onset of atherosclerosis through lowering the low-density lipoproteins and mechanisms associated with inflammatory induction of plaque accumulation on the arterial wall.

Dr. Jang YJ, the lead scientist wrote, “sinigrin decreases the TNF-α-stimulated VCAM-1 expression through the suppression of NF-κB and MAP kinases signaling pathways, Overall, sinigrin has the potential to be used in reducing the risks of atherosclerosis”.

Taken altogether, sinigrin may be considered a supplement for the prevention and combined with the primary therapy for the treatment of atherosclerosis, pending to the confirmation 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.

Sources
(1) Sinigrin attenuates the progression of atherosclerosis in ApoE-/- mice fed a high-cholesterol diet potentially by inhibiting VCAM-1 expression by Jang YJ1, Park B1, Lee HW1, Park HJ1, Koo HJ2, Kim BO3, Sohn EH4, Um SH5, Pyo S. (PubMed)
(2) Western Diet Increases Inflammatory Responses and Atherosclerosis Progression via IGF-1 Receptor in ApoE-Deficient Mice by Meifang Wang, Yusuke Higashi, Derek Wang, Ronald Korthuis, and Patrice Delafontaine. (FASEB Journal)