Taxifolin Reduces Blood Pressure via Improvement of Vascular Function and Mitigating the Vascular Inflammatory Response in Spontaneously Hypertensive Rats

Abstract

The effect of a 10-day-long treatment with taxifolin (TAX, 20 mg/kg/day p.o.) was investigated on spontaneously hypertensive rats (SHRs) with a focus on the vascular functions of isolated femoral arteries and thoracic aortas. TAX reduced blood pressure in SHRs. In femoral arteries, TAX increased acetylcholine-induced relaxation, reduced the maximal NA-induced contraction, and reduced acetylcholine-induced endothelium-dependent contraction (EDC); however, TAX had no effect on the vascular reactivity of isolated thoracic aortas. In addition, TAX elevated the total nitric oxide synthase (NOS) activity and iNOS protein expression but reduced cyclooxygenase-2 (COX2) protein expression in the tissue of the abdominal aorta without changes in Nos2 and Ptgs2 gene expressions. TAX also increased the gene expression of the anti-inflammatory interleukin-10 (Il10). In addition, in vitro studies showed that TAX has both electron donor and H atom donor properties. However, TAX failed to reduce superoxide production in the tissue of the abdominal aorta after oral administration. In conclusion, our results show that a decrease in the blood pressure in TAX-treated SHRs might be attributed to improved endothelium-dependent relaxation and reduced endothelium-dependent contraction. In addition, the results suggest that the effect of TAX on blood pressure regulation also involves the attenuation of COX2-mediated pro-inflammation and elevation of anti-inflammatory pathways.

Ca2+-Dependent Cl− Channels in Vascular Tone Regulation during Aging

“…Since the [Cl − ]i of endothelial cells is slightly lower than that of VSMC, and the equilibrium potential for Cl − of endothelial cells is unknown, the activation of CaCCs leaves open two possibilities, i.e., that CaCCs may promote depolarization and nitric oxide (NO) release from intact endothelium, or that CaCCs may cause hyperpolarization (Figure 1). NO is produced by NOS from L-arginine, and various mechanisms deploy their beneficial effects through the activation of endothelial NOS [44][45][46][47] or the inhibition of inducible NOS [48]. TMEM16A on endothelial cells are localized not only at the plasma membrane but also at the mitochondrial membrane; thus, it is important to distinguish which channels are influenced while carrying out a study with CaCCs.…”

A Comparative Study of the Inhibitory Effect of Some Flavonoids and a Conjugate of Taxifolin with Glyoxylic Acid on the Oxidative Burst of Neutrophils

“…The consumption of polyphenol-rich foods and beverages may be associated with a reduction of the risk of cardiovascular [1][2][3], neurodegenerative [4][5][6][7], and some other diseases [8,9]. Polyphenols show a broad spectrum of biological activities, including antioxidant [10,11], anti-inflammatory [12], antibacterial [13], antiplatelet [14][15][16][17], antihypertensive [18][19][20][21], and anticarcinogenic activities [22]. Polyphenols are highly varied in structure, but all of them contain at least one benzene ring bearing several hydroxyl groups [23].…”