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Inflammation, Oxidative Stress, and Cerebral Stroke: Basic Principles

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Advancement in the Pathophysiology of Cerebral Stroke

Abstract

Cerebral stroke has assorted causes, disrupting the cerebral blood flow and subsequently damaging the brain tissues in affected areas. Stroke is the third primary cause of death and disability in adults around the globe. In approximately 25–40% of cerebral stroke patients, the neurological signs are initiated during the early hours. The mechanism involved in the pathophysiology of cerebral stroke are oxidative stress and inflammation. Oxidative stress takes place when there is an impairment to the balance of antioxidant generation with reactive oxygen species (ROS) and other free radicals/oxidants. The brain is extremely vulnerable to oxidative stress owing to the high consumption of body oxygen to produce energy and free radicals, which may cause damage to the main cellular components, such as lipids, proteins, and DNA, and contributing to late-stage apoptosis and inflammation. Inflammation plays significant role in the pathogenesis of cerebral stroke and associated brain damage. Experimentally and clinically, ischemic brain injury takes place because of the initiation of severe and extended inflammatory progression. These processes include activation of brain microglial cells, production of pro-inflammatory mediators (cytokines and chemokines), and infiltration of numerous inflammatory cells such as neutrophils, T-cells, monocyte/macrophages, and natural killer cells into the ischemic brain regions, which initiates neuronal injuries and cell death mechanisms. In this chapter, we focus on the cellular and molecular evidence for oxidative stress and inflammation in cerebral stroke. In addition, we highlight certain current findings and knowledge of the neuroprotective strategies that target oxidative stress/inflammation and their implications in the pathogenesis of cerebral stroke.

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Abbreviations

BBB:

Blood–brain barrier

NO:

Nitric oxide

RNS:

Reactive nitrogen species

ROS:

Reactive oxygen species

SOD:

Superoxide dismutase

TNF:

Tumor necrosis factor

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Correspondence to Shashi Kant Tiwari .

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Tiwari, S.K., Mishra, P., Rajavashisth, T. (2019). Inflammation, Oxidative Stress, and Cerebral Stroke: Basic Principles. In: Patnaik, R., Tripathi, A., Dwivedi, A. (eds) Advancement in the Pathophysiology of Cerebral Stroke. Springer, Singapore. https://doi.org/10.1007/978-981-13-1453-7_2

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