Protective effects of hydroxysafflor yellow A on acute and chronic congestive cardiac failure mediated by reducing ET-1, NOS and oxidative stress in rats RETRACTED ARTICLE

Abstract

The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect on acute and chronic heart failure (AHF/CHF) induced by ligation of the left anterior descending coronary artery for 3 h and 8 weeks, respectively. The rats were divided into the following groups: sham operation, coronary artery ligation (CAL), CAL+HSYA (100 mg kg(-1) by gavage) and CAL+diltiazem (20 mg kg(-1) by gavage). In the AHF model, heart function, as determined by haemodynamic studies and echocardiography, was improved significantly by pretreatment with HSYA or diltiazem. Significant reductions in elevated serum creatine phosphokinase, lactate dehydrogenase, malondialdehyde (MDA), glutamic oxalacetic transaminase, glutamic pyruvic transaminase and blood viscosity were observed, and the activity of serum superoxide dismutase (SOD) was enhanced (all P<0.01). In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD. HSYA and diltiazem improved cardiac performance in AHF and reduced cardiac remodelling in CHF by reducing tissue weight indices: left ventricular weight/body weight (BW), right ventricular weight/BW, kidney weight/BW and lung weight/BW, and attenuating increases in infarct size, inner diameter of the left ventricle and collagen volume fraction in non-infarcted areas, and the decrease in mean wall thickness of infarcted myocardium. These results suggest that HSYA exerted beneficial actions in cardiac performance in models of both AHF and CHF, mainly by suppressing ET-1, iNOS and oxidative stress in infarcted tissue.

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet by regulating PPAR-γ/p38 MAPK signaling

“…Previous studies have demonstrated that the protective effect of HSYA against LPS-induced acute lung injury was associated with the significant inhibition of p38 MAPK phosphorylation in vitro and in vivo (Song et al, 2013;Sun et al, 2010). He et al (2008) revealed that the non-receptor tyrosine phosphatase Shp2 promotes adipogenesis through the Shp2-p38MAPK-p300-PPARg signaling pathway, by inhibiting the phosphorylation of p38 MAPK and enhancing PPAR-g expression. Consistent with this, the PPAR-g agonist rosiglitazone has been shown to downregulate gonadotropin-releasing hormone-mediated phosphorylation of p38 MAPKs in LbT2 cells (Sakaida et al, 2004).…”

Hydroxysafflor Yellow A Protects PC12 Cells Against the Apoptosis Induced by Oxygen and Glucose Deprivation

“…It has been reported that free radicals play an active role in the early events of OGD-R-induced apoptosis (Rawal et al 2004;Shen et al 2004). It has been reported that HSYA, one of the major active chemical component of the yellow color pigments extracted from the safflower, exhibits strong scavenging effects on cytotoxic oxygen radicals (Tian et al 2008;Wei et al 2005;He et al 2008). In the present experiment, OGD-R caused a significant increase in level of MDA, the marker of lipid peroxidation.…”

Coordinated Activation of VEGF/VEGFR-2 and PPARδ Pathways by a Multi-Component Chinese Medicine DHI Accelerated Recovery from Peripheral Arterial Disease in Type 2 Diabetic Mice

“…It exerts a variety of effects upon the cardiovascular system. For example, HSYA inhibits thrombosis and platelet aggregation, improves congestive cardiac failure in rats by suppressing ET-1 and iNOS and reduces oxidative stress in infarcted tissue [23]. HSYA has also been shown to reduce phenylephrine or KCl-induced vasoconstriction and to reduce blood pressure and heart rate [24].…”