Pretreatment With Beta-Boswellic Acid Improves Blood Stasis Induced Endothelial Dysfunction: Role Of Enos Activation

Vascular endothelial cells play an important role in modulating anti-thrombus and maintaining the natural function of vascular by secreting many active substances. beta-boswellic acid (beta-BA) is an active triterpenoid compound from the extract of boswellia serrate. In this study, it is demonstrated that beta-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 beta-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 beta-BA significantly increased intracellular NO level. Western blot and immunofluorescence as well as immunohistochemistry reveal that beta-BA increases phosphorylation of enzyme nitric oxide synthase (eNOS) at Ser1177. In addition, beta-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 beta-BA is attenuated by knockdown of eNOS. In conclusion, the above findings provide convincing evidence for the protective effects of beta-BA on blood stasis induced endothelial dysfunction by eNOS signaling pathway.