![]() ![]() 12 Taurine, which is another potent antioxidant that is found in food, has been reported to protect against endothelial damage. 11 Polyphenols may also stimulate endogenous antioxidant enzymes and inhibit xanthine and nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidases. 10 β-carotene prevents the oxidative modification of low-density lipoprotein cholesterol. Vitamin E and C have antioxidant and membrane stabilizing functions. On the other hand, the long-term ingestion of foods that contain high levels of antioxidants also acts to protect against oxidative stress. 9 Thus, the administration of ARBs and statins, which have an antioxidative effect, is an effective therapeutic strategy that promotes the repair of cardiovascular damage by enhancing the repair of endothelial damage by EPCs. We also recently demonstrated that basal EPC function was inversely correlated with blood pressure and impaired in patients with essential hypertension, and that treatment with an ARB significantly improved their impaired EPC function. 4 We have demonstrated that the formation and function of EPCs is impaired in hypertensive rats with increases in oxidative stress and that treatment with angiotensin II receptor blockers (ARBs) 5, 6, 7 and a hydroxymethylglutaryl-CoA reductase inhibitor statin 8 apparently improved the impaired function of EPCs by suppressing oxidative stress in spontaneously hypertensive rats (SHR). Accumulating evidence indicates that reactive oxygen species have major roles in the initiation and progression of the cardiovascular dysfunction associated with diseases such as hyperlipidemia, diabetes mellitus, hypertension and ischemic heart disease. ![]() ![]() 3 Hence, it is more likely that the pathway controlling EPC release is downregulated by the presence of risk factors rather than by the consumption of EPCs. EPC numbers have also been shown to be reduced in patients with other disorders who are at higher risk for cardiovascular diseases. 2 demonstrated a reduction of EPC colony formation in healthy individuals with risk factors for cardiovascular disease. Taurine and Mg supplementation increased EPC colony formation in healthy men and improved impaired EPC function in SHRs through antioxidation, indicating that the dietary intake of taurine and Mg may prolong lifespan by preventing the progression of cardiovascular diseases.Įndothelial progenitor cells (EPCs) induce angiogenesis, neovascularization and endothelial repair by homing in on sites of endothelial damage. Nicotinamide adenine dinucleotide phosphate oxidase component mRNA expression was significantly higher in the renal cortex of salt-loaded SHRs than in WKY rats, in which it was suppressed by taurine and Mg supplementation. Taurine and Mg supplementation significantly increased EPC colony numbers and significantly decreased TBARS scores and free radical levels in SHRs. Taurine and Mg supplementation significantly increased EPC colony numbers and significantly decreased free radical levels and TBARS scores in healthy men. Oxidative stress markers in their peripheral blood were evaluated using a free radical analytical system and a thiobarbituric acid reactive substance (TBARS) assay. Their peripheral blood mononuclear cells were separated to quantify EPC colony formation. ![]() The SHRs received 3% taurine solution and/or a high-Mg (600 mg per 100 g) diet for 4 weeks. SHRs and Wistar-Kyoto (WKY) rats were housed with high-salt drinking water (1% NaCl). Healthy men received taurine (3 g per day) or Mg (340 mg per day) for 2 weeks. We herein evaluate the effects of taurine and Mg supplementation on EPC function and oxidative stress in healthy men and spontaneously hypertensive rats (SHRs). The WHO Cardiovascular Diseases and Alimentary Comparison Study demonstrated that dietary taurine and magnesium (Mg) intake suppresses cardiovascular diseases. Endothelial damage is repaired by endothelial progenitor cells (EPCs), which are pivotal in preventing cardiovascular diseases and prolonging lifespan. ![]()
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