Mapanga et al. explored that oleanolic acid, an antioxidant agent that blunts hyperglycemia-induced contractile dysfunction. In consistent with the previous report, in this study L-NAME induction reduces the contractile function and SA treatment restores the ventricular function with its antioxidant property. The protection of vascular function by SA was one of the significant findings of this study. Vascular endothelium plays a pivotal role in the pathophysiology of cardiovascular system. Nitric oxide, generated by eNOS, is physiologically important in vascular homeostasis, which readily activates guanylyl cyclase and increases cyclic GMP formation in vascular smooth muscle. Endogenous NO reacts with superoxide to form peroxynitrite, which is capable of either oxidizing or nitrating various biological substrates. Previous study illustrates that, AbMole BioScience pioglitazone administration reduced oxidative stress, prevented breakdown of NO and increased NO levels, thereby restoring the endothelial function in aorta of diabetic rat. In the current study, decreased response of aorta to Ach induced endothelium dependent relaxations occurred in L-NAME induced hypertensive rats might be due to the reduced production/bioavailability of NO and elevated oxidative stress. Moreover, in the present study eNOS mRNA and protein expressions were down regulated coupled with increased ACE activity in the aorta of L-NAME rats whereas SA restored the above. In a Ruxolitinib clinical trial similar study, LNAME treated rats showed definite increase in systolic blood pressure, decrease in eNOS gene expression in aortic tissue and decreased response of aorta to acetylcholine. Further, ACE inhibition by enalapril or quinapril was equally effective in improving endothelial vasodilator function and restoring aortic eNOS mRNA. Likewise, protective action of SA might be due to increased NO level and decreased ACE activity through antioxidant potential, which was strongly supported by our in vitro endothelial cell culture study. In order to support our in vivo results obtained from isolated aortic ring experiments in organ bath system, we analyzed the protective effect of SA on endothelial cell injury induced by H2O2 in vitro. In this study, we demonstrated that H2O2 could markedly increase cell death, induce oxidative stress and decline NO production. The up-regulation of ROS in vascular lesions will exert detrimental effects on the peroxidation of membrane lipids, endothelium-derived enzyme inactivation, apoptotic occurrences, etc. In contrast, antioxidants/ agents that react preferentially with ROS to inactivate them or enhance cellular antioxidant defenses can protect cells from the damaging effects of oxygen radicals. Observations of a former study on the current model have provide preliminary evidence that antioxidant TSN IIA protects EA.hy926 cells against H2O2 damage, which is mainly associated with the ROS generation. Similarly, our study showed that SA not only reduced the intracellular ROS induced by H2O2, but also effectively increase cell viability and NO level in H2O2-induced endothelial cells, which shows the protective potential of SA on endothelial cells. In conclusion, hypertensive rats treated with SA demonstrated attenuated hypertension and improved cardiovascular function. SA treatment reduced the oxidative stress and myocardial fibrosis observed in hypertensive rats. These findings suggest that SA may have great therapeutic potential in the treatment of hypertensive heart disease. We previously reported that in ALK+ ALCL, ALK protein induces the expression of the transcription factor C/EBP�� primarily through STAT3, and that C/EBP�� plays a central role in ALK-mediated oncogenesis.