Open Access

Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats

  • Authors:
    • Xian‑Liang Meng
    • Dong‑Lin Zhang
    • Shi‑Hua Sui
  • View Affiliations

  • Published online on: July 19, 2019     https://doi.org/10.3892/etm.2019.7797
  • Pages: 1953-1960
  • Copyright: © Meng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


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.
View Figures
View References

Related Articles

Journal Cover

September-2019
Volume 18 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Meng XL, Zhang DL and Sui SH: Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats. Exp Ther Med 18: 1953-1960, 2019
APA
Meng, X., Zhang, D., & Sui, S. (2019). Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats. Experimental and Therapeutic Medicine, 18, 1953-1960. https://doi.org/10.3892/etm.2019.7797
MLA
Meng, X., Zhang, D., Sui, S."Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats". Experimental and Therapeutic Medicine 18.3 (2019): 1953-1960.
Chicago
Meng, X., Zhang, D., Sui, S."Acute remote ischemic preconditioning alleviates free radical injury and inflammatory response in cerebral ischemia/reperfusion rats". Experimental and Therapeutic Medicine 18, no. 3 (2019): 1953-1960. https://doi.org/10.3892/etm.2019.7797