Inflammation in Ischemic Stroke: Mechanisms, Consequences and Possible Drug Targets

Title:Inflammation in Ischemic Stroke: Mechanisms, Consequences and Possible Drug Targets

Volume: 13 Issue: 8

Author(s): Muzamil Ahmad, Nawab J. Dar, Zubair S. Bhat, Aehtesham Hussain, Ayatullah Shah, Hao Liu and Steven H. Graham

Affiliation:

Keywords: Cerebral ischemia, cyclooxygenase-2, cytokines and chemokines, inflammation, microglia, middle cerebral artery occlusion, prostaglandin.

Abstract: Ischemic stroke is caused when blood flow to the brain is hampered, leading to instant deficiency of nutrients and oxygen required for normal brain functioning. Reperfusion can alleviate damage from stroke if performed immediately after the onset of ischemia however the efficacy of reperfusion is tempered by secondary injury mechanisms. This multifarious sequence of events leads to the commencement of deleterious cycles of inflammation, oxidant stress and apoptosis that finally culminate in delayed death of neuronal cells even when the brain is effectively reperfused. Wealth of data from clinical as well as experimental studies points to a prominent role of inflammation in secondary injury. In this review we will discuss, in detail, the cellular and molecular mediators of inflammation and their possible therapeutic targets in both experimental and clinical forms of stroke.

Cite this article as:

Ahmad Muzamil, Dar J. Nawab, Bhat S. Zubair, Hussain Aehtesham, Shah Ayatullah, Liu Hao and Graham H. Steven, Inflammation in Ischemic Stroke: Mechanisms, Consequences and Possible Drug Targets, CNS & Neurological Disorders - Drug Targets 2014; 13 (8) . https://dx.doi.org/10.2174/1871527313666141023094720