Cardiovascular diseases (CVDs) such as angina, hypertension, myocardial ischemia, and heart failure are the leading causes of morbidity and mortality worldwide. One of the major transcription factors widely associated with CVDs is nuclear factor-kappa B (NFκB). NFκB activation initiates the canonical and non-conical pathways that promotes activation of transcription factors leading to inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. Flavonoids are bioactive polyphenolic compounds found abundantly in various fruits, vegetables, beverages (tea, coffee), nuts, and cereal products with cardiovascular protective properties. Flavonoids can be classified into six subgroups based on their chemical structures: flavanones, flavones, flavonols, flavan-3-ols, isoflavones, and anthocyanidins. As NFκB inhibitors, these flavonoids may modulate the expression of pro-inflammatory genes leading to the attenuation of the inflammatory responses underlying various cardiovascular pathology. This review presents an update on the anti-inflammatory actions of flavonoids via inhibition of NFκB mechanism supporting the therapeutic potential of these natural compounds in various CVDs.

Hypertension and atherosclerosis are among the most common causes of mortality in both developed and developing countries. Experimental animal models of hypertension and atherosclerosis have become a valuable tool for providing information on etiology, pathophysiology, and complications of the disease and on the efficacy and mechanism of action of various drugs and compounds used in treatment. An animal model has been developed to study hypertension and atherosclerosis for several reasons. Compared to human models, an animal model is easily manageable, as compounding effects of dietary and environmental factors can be controlled. Blood vessels and cardiac tissue samples can be taken for detailed experimental and biomolecular examination. Choice of animal model is often determined by the research aim, as well as financial and technical factors. A thorough understanding of the animal models used and complete analysis must be validated so that the data can be extrapolated to humans. In conclusion, animal models for hypertension and atherosclerosis are invaluable in improving our understanding of cardiovascular disease and developing new pharmacological therapies.

This review is to examine the current literatures on the relationship between periodontitis and hypertension as well as to explore the possible biological pathways underlying the linkage between these health conditions. Hypertension is one of the major risk factors for cardiovascular diseases. Oxidative stress and endothelial dysfunction are among the critical components in the development of hypertension. Inflammation has received much attention recently and may contribute to a pivotal role in hypertension. Periodontitis, a chronic low-grade inflammation of gingival tissue, has been linked to endothelial dysfunction, with blood pressure elevation and increased mortality risk in hypertensive patients. Inflammatory biomarkers are increased in hypertensive patients with periodontitis. Over the years, various researches have been performed to evaluate the involvement of periodontitis in the initiation and progression of hypertension. Many cross-sectional studies documented an association between hypertension and periodontitis. However, more well-designed prospective population trials need to be carried out to ascertain the role of periodontitis in hypertension.

Cardiovascular diseases such as hypertension and atherosclerosis are the common causes of mortality in developed and developing countries. Repeated heating of the dietary oil is a common practice to reduce cost during food preparation. When the cooking oil is heated at high temperatures, production of free radicals augments the oxidative degradation of lipids and depletes the natural antioxidant contents of the cooking oil. Chronic intake of foods prepared using reheated oil could impair antioxidant capacity, leading to oxidative stress and inflammation. This review aims to summarize the current evidence of lipid oxidation products on hypertension and atherosclerosis via inflammatory pathway. In particular, toxic lipid oxidation products such as malondialdehyde and 4-hydroxy-2-nonenal are taken into account. Understanding the signaling pathways underlying the pathology associated with the lipid oxidation-derived aldehydes may be useful to develop therapeutic strategies for the prevention of inflammatory-related cardiovascular complications.

Hypertension increases the risk for a variety of cardiovascular diseases, including stroke, coronary artery disease, heart failure, and peripheral vascular disease. The increase in oxidative stress has been associated with the pathogenesis of hypertension. Increase of blood pressure is due to an imbalance between antioxidants defence mechanisms and free radical productions. Excessive production of reactive oxygen species reduces nitric oxide bioavailability leading to an endothelial dysfunction and a subsequent increase in total peripheral resistance. Hypertension can cause few symptoms until it reaches the advanced stage and poses serious health problems with lifelong consequences. Hypertensive patients are required to take drugs for life to control the hypertension and prevent complications. Some of these drugs are expensive and may have adverse reactions. Hence, it is timely to examine scientifically, complimentary therapies that are more effective and with minimal undesirable effects.Nigella sativa(NS) and its active constituents have been documented to exhibit antioxidant, hypotensive, calcium channel blockade and diuretic properties which may contribute to reduce blood pressure. This suggests a potential role of NS in the management of hypertension, and thus more studies should be conducted to evaluate its effectiveness.