Quercetin in the Pure Quercetin Powder is one of the more widely studied flavonoids, and its powerful antioxidant and anti-inflammatory activities have been fully proved, with strong biological activities and extensive pharmacological effects. Quercetin has a therapeutic effect on cardiovascular diseases, but because of its extremely low water solubility, poor oral absorption, and low bioavailability, the research and application of quercetin in new dosage forms of cardiovascular diseases have also attracted more and more attention.
Studies have found that quercetin can inhibit myocardial hypertrophy and improve diastolic function in abdominal aortic coarctation. In primary cardiomyocytes, quercetin can significantly reduce the surface area and atrial natriuretic factor of angiotensin II-induced cardiomyocyte hypertrophy. mRNA levels, while quercetin can increase the activity of proteasome GSK3. In spontaneously hypertensive rats, quercetin attenuated hypertensive disease and significantly reduced the ratio of the left ventricle to body weight.
In vitro experiments found that quercetin can concentration-dependently inhibit leucine incorporation into H9C2 cells and reduce the surface area of mast cells, indicating that quercetin can effectively inhibit angiotensin II-induced hypertrophy of H9C2 cells. In addition, inhibition of cardiac hypertrophy can effectively reduce the mortality of the cardiovascular disease. The ratio of cardiac weight increased in rats in the 3-week postoperative abdominal aortic coarctation group compared with the sham-operated rats, while the myocardial Hypertrophy was completely inhibited and the associated malondialdehyde production was significantly reduced. In the model group, the activities of ERK1/2, p38 MAPK, Akt, and GSK-3β were significantly increased with the increase of pressure load. After treatment with quercetin, the activities of these proteins were inhibited, indicating that quercetin can inhibit stress-induced myocardial hypertrophy. development and protects by reducing oxidative stress and inhibiting the activity of ERK1/2, p38 MAPK, Akt, and GSK-3β.
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