Traditional Chinese medicine xin-mai-jia recouples endothelial nitric oxide synthase to prevent atherosclerosis in vivo

Abstract

Endothelial dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial step in atherosclerosis. This study was designed to explore whether Chinese medicine xin-mai-jia (XMJ) recouples eNOS to exert anti-atherosclerotic effects. Pretreatment of XMJ (25, 50, 100 μg/ml) for 30 minutes concentration-dependently activated eNOS, improved cell viabilities, increased NO generations, and reduced ROS productions in human umbilical vein endothelial cells incubated with H2O2 for 2 hours, accompanied with restoration of BH4. Importantly, these protective effects produced by XMJ were abolished by eNOS inhibitor L-NAME or specific eNOS siRNA in H2O2-treated cells. In ex vivo experiments, exposure of isolated aortic rings from rats to H2O2 for 6 hours dramatically impaired acetylcholine-induced vasorelaxation, reduced NO levels and increased ROS productions, which were ablated by XMJ in concentration-dependent manner. In vivo analysis indicated that administration of XMJ (0.6, 2.0, 6.0 g/kg/d) for 12 weeks remarkably recoupled eNOS and reduced the size of carotid atherosclerotic plaque in rats feeding with high fat diet plus balloon injury. In conclusion, XMJ recouples eNOS to prevent the growth of atherosclerosis in rats. Clinically, XMJ is potentially considered as a medicine to treat patients with atherosclerosis.

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

“…As a result, we would expect that VitB6 may suppress inflammation in culture macrophages. Inflammation was induced by LPS and assessed by measuring the levels of inflammatory cytokines, such as TNF‐α and IL‐1β, which are the inflammatory makers . As depicted in, treatment of cultured macrophages with LPS for 24 hours dramatically induced the secretion of both TNF‐α, IL‐1β and IL‐6 as increased levels in cultured medium by ELISA (Figure A‐C), as well as increased gene expressional levels in total cells by real‐time PCR (Figure D‐F).…”

“…Inflammation was induced by LPS and assessed by measuring the levels of inflammatory cytokines, such as TNF-α and IL-1β, which are the inflammatory makers. 20,26 As depicted in, treatment of cultured macrophages with LPS for 24 hours dramatically induced the secretion of both TNF-α, IL-1β and IL-6 as increased levels in cultured medium by ELISA (Figure 2A…”

Administration of losartan improves aortic arterial stiffness and reduces the occurrence of acute coronary syndrome in aged patients with essential hypertension

“…Several mechanisms may explain our finding of an association between increased PWV and ACS. Various pharmacological approaches have been recommended for obtaining a pressure-independent reduction in arterial stiffness, including the blockade of the RAAS, smooth muscle cell relaxation by nitric oxide donors or related molecules including statin and traditional Chinese medicine, [29][30][31][32][33] targeting of molecular events leading to arterial stiffening, or interference with collagen metabolism. A growing body of in vitro studies shows that cyclic stretching exerts a greater influence than the static load on phenotype and growth of vascular smooth muscle cells.…”

Perillaldehyde prevents the formations of atherosclerotic plaques through recoupling endothelial nitric oxide synthase

“…12 At the end of experiment, rats were killed by anesthetizing with an intraperitoneal injection of 0.8% pentobarbital sodium (60 mg/kg), followed by cervical dislocation. Four weeks after HFD, rats were injected with vitamin D3 and received balloon injury in carotid artery as described previously.…”