Abstract
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.
Highlights
Cardiovascular diseases (CVDs) represent the major burden of mortality and morbidity in the developed countries (Benjamin et al, 2017)
In LPS-challenged apoE-/- mice, treatment with apigenin increased expression of ATP binding cassette A1 (ABCA1), which alleviated extra lipid accumulation, reduced miR-33, toll-like receptor 4 (TLR-4), and NFκB p65 levels, lessened the macrophages and smooth muscle cell contents in the atherosclerotic region, and improved plasma lipid profile (Ren et al, 2018). These results suggested that apigenin attenuates atherogenesis by inhibition of nuclear NFκB p65 that up-regulates ABCA1-mediated cholesterol efflux (Ren et al, 2018)
In a rat model of myocardial infarction, fibrosis in the interstitial and perivascular regions and expression of collagen was reduced following chrysin treatment (Yang et al, 2018). This effect is associated with increased PPAR-γ expression and decreased NFκB expression via inhibition of IκKβ phosphorylation, leading to reduction of matrix metalloproteinase-2 (MMP-2), MMP-9 levels, and suppression of activator protein 1 (AP-1) level
Summary
Cardiovascular diseases (CVDs) represent the major burden of mortality and morbidity in the developed countries (Benjamin et al, 2017). The most common pathogeneses of CVDs are inflammatory processes (Ruparelia et al, 2017). Various transcription factors are related to inflammatory responses in CVDs such as T-bet (Haybar et al, 2019), signal transducer and activator of transcription 3 (STAT3) (Kurdi et al, 2018), interferon regulatory factors (IRFs), activator protein 1 (AP-1) (Smale and Natoli, 2014), and transcription factor Bcl11b (Daher et al, 2019). The key player in the regulation of inflammation is the transcription factor nuclear factor kappa B (NFκB) (Van Der Heiden et al, 2010)
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