Abstract
Vascular endothelial cells play an important role in modulating anti-thrombus and maintaining the natural function of vascular by secreting many active substances. β-boswellic acid (β-BA) is an active triterpenoid compound from the extract of boswellia serrate. In this study, it is demonstrated that β-BA ameliorates plasma coagulation parameters, protects endothelium from blood stasis induced injury and prevents blood stasis induced impairment of endothelium-dependent vasodilatation. Moreover, it is found that β-BA significantly increases nitric oxide (NO) and cyclic guanosine 3’, 5’-monophosphate (cGMP) levels in carotid aortas of blood stasis rats. To stimulate blood stasis-like conditions in vitro, human umbilical vein endothelial cells (HUVECs) were exposed to transient oxygen and glucose deprivation (OGD). Treatment of β-BA significantly increased intracellular NO level. Western blot and immunofluorescence as well as immunohistochemistry reveal that β-BA increases phosphorylation of enzyme nitric oxide synthase (eNOS) at Ser1177. In addition, β-BA mediated endothelium-dependent vasodilatation can be markedly blocked by eNOS inhibitor L-NAME in blood stasis rats. In OGD treated HUEVCs, the protective effect of β-BA is attenuated by knockdown of eNOS. In conclusion, the above findings provide convincing evidence for the protective effects of β-BA on blood stasis induced endothelial dysfunction by eNOS signaling pathway.
Highlights
Endothelium plays a predominant role in maintaining vascular homeostasis by means of modulation[9]
In order to explore the beneficial properties of boswellia serrata and the possible roles of enzyme nitric oxide synthase (eNOS)-Nitric oxide (NO)– cyclic guanosine monophosphate (cGMP) pathway, it is hypothesized that β -BA can provide endothelium protection against vascular injury induced by blood stasis syndrome in rats and oxygen and glucose deprivation (OGD) in human umbilical vein endothelial cells (HUVECs)
Mesenteric artery rings from blood stasis treated animals showed reduced endothelium-dependent vasodilator responses to acetylcholine in artery rings stimulated by phenylephrine compared to control aortic rings ACh-mediated vessel relaxation was significantly improved in β -BA (100 mg/kg/d) and β -BA (200 mg/kg/d) groups compared with blood stasis rats (Fig. 1a). β -BA prevented the blood stasis induced impairment of endothelium-dependent vasodilatation
Summary
Endothelium plays a predominant role in maintaining vascular homeostasis by means of modulation[9]. Nitric oxide (NO), an antithrombotic product for endothelial cells, plays a crucial role in vascular homeostasis. It inhibits the aggregation of platelets and prevents adhesion of platelets to endothelium, and thereby prolongs the bleeding time[14] and reduces the plasma levels of fibrinogen[14]. The constitutive calcium-calmodulin-dependent enzyme nitric oxide synthase (eNOS) is key for synthesization of NO from the amino acid L-arginine in endothelial cells[17,18]. It seems that phosphorylation of eNOS at Ser1177 is the most important site for eNOS activity regulation. In order to explore the beneficial properties of boswellia serrata and the possible roles of eNOS-NO– cGMP pathway, it is hypothesized that β -BA can provide endothelium protection against vascular injury induced by blood stasis syndrome in rats and oxygen and glucose deprivation (OGD) in human umbilical vein endothelial cells (HUVECs)
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