No abstract

Remote ischemic preconditioning (IPreC) is an effective strategy to defend against cerebral ischemia/reperfusion (IR) injury; however, its mechanisms remain to be elucidated. The aim of the present study was to investigate the effect of IPreC on brain tissue following cerebral ischemia, as well as the underlying mechanisms. Adult male Sprague-Dawley rats were treated with IPreC for 72 h prior to the induction of transient cerebral ischemia and reperfusion. The results demonstrated that IPreC reduced the area of cerebral infarction in the IR rats by 2,3,5-triphenyl-tetrazolium chloride staining. In addition, cell apoptosis was markedly suppressed by IPreC with an increased expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associatd X protein using Terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay and western blot analysis. IR induced a decrease in the level of superoxide dismutase, and IPreC significantly suppressed increased levels of malondialdehyde, lactate dehydrogenase and nitric oxide. The expression of CD11b and CD18 was markedly inhibited by IpreC unsing flow cytometry. Furthermore, IPreC markedly decreased the release of pro-inflammatory factors interleukin (IL)-6 and IL-1β, and enhanced the level of anti-inflammatory factors (IL-10 and IL-1 receptor antagonist) by ELISA assay. Finally, IPreC reduced the levels of transforming growth factor-β-activated kinase 1, phosphorylated-P65/P65, and tumor necrosis factor-α, indicating that the nuclear factor-κB pathway was involved in IPreC-mediated protection against cerebral ischemia. Taken together, the results suggested that IPreC decreased ischemic brain injury through alleviating free radical injury and the inflammatory response in cerebral IR rats.

Abstract. Arteriosclerosis poses a significant risk to human health and involves the thickening and hardening of the walls of arteries. Accumulated evidence demonstrates that aberrant proliferation of vascular smooth muscle cells (VSMCs) accounts for the onset and progression of arteriosclerosis. Suppression of their proliferation has been demonstrated to be an effective anti-arteriosclerosis strategy. Long non-coding RNAs (lncRNAs) have recently been observed to be implicated in the proliferation of VSMCs and arteriosclerosis. In this study, we observed that oleanolic acid (OA), a natural compound from plants, inhibited the proliferation of VSMCs. The expression of lincRNA-p21, an arteriosclerosis-associated lncRNA, was demonstrated to be elevated by OA treatment. Suppression of lincRNA-p21 rescued the effect of OA on the proliferation of VSMCs. Collectively, targeting lncRNA is a promising strategy for arteriosclerosis prevention and treatment, and OA ameliorates arteriosclerosis by increasing lncRNA levels.