Cerebral Ischemia Reperfusion Injury

Authors

  • Najah R. Hadi Faculty of Medicine University of Kufa, Iraq.
  • Saif M. Hassan Pharmacology and therapeutics, Al Zahrawi University College, Iraq.
  • Mahmood J. Jawad Pharmacology and therapeutics, Al Zahrawi University College, Iraq.
  • Wajdy Alawaida Department of Biology and Biotechnology, American University of Madaba, Madaba, Jordan, P. O. Box: 2882 Amman 11821 Jordan.

DOI:

https://doi.org/10.9734/bpi/mono/978-93-91473-00-6

Keywords:

Cerebral ischemia reperfusion, Nf-kb, Nrf2, Nrf2 activators, neuroprotective

Abstract

Ischemia-reperfusion injury is a common feature of ischemic stroke, which occurs when blood supply is restored after a period of ischemia. Reperfusion can be achieved either by Thrombolysis using thrombolytic reagents such as tissue plasminogen activator (tPA), or through mechanical removal. Cerebral ischemia can induce inflammation with generation of Nf-kb, adhesion molecules, and upregulation of toll-like receptors while reperfusion generates reactive oxygen species (ROS) and opening of mitochondrial pore as well as inflammation and apoptosis. Nrf2 has neuroprotective role via increasing gene expression of anti-oxidant elements as well as anti-inflammatory effects. Further, Nrf2 activators were found to inhibit HMGB1 induced inflammation and ROS induce cerebral damage, as well as reduce p38 MAPK upregulation that can reduce NF-kB expression.

Published

2021-07-02

How to Cite

Najah R. Hadi, Saif M. Hassan, Mahmood J. Jawad, & Wajdy Alawaida. (2021). Cerebral Ischemia Reperfusion Injury. Cerebral Ischemia Reperfusion Injury, 1–63. https://doi.org/10.9734/bpi/mono/978-93-91473-00-6

Issue

Cerebral Ischemia Reperfusion Injury

Section

Content