Inflammation in the pathogenesis of ischemic stroke

Abstract

Ischemic stroke is a common cause of permanent disability in adults worldwide. Inflammation plays a significant role in the pathogenesis of ischemic stroke and its mechanism is complex. Both pro-inflammatory and anti-inflammatory mediators are involved in the pathogenesis of ischemic stroke, an imbalance of which leads to inflammation. Inflammatory cells from both the innate and acquired immune systems are involved in ischemic stroke-related inflammation; processes that are linked by the action of interleukin-17A (IL-17A). Although most inflammatory cells promote inflammation, T regulatory cells (Tregs) may have a protective function at the early stages of an ischemic injury, but a negative role during later stages. However, the precise mechanism of inflammation in ischemic stroke remains elusive; further understanding of it may provide new ideas for the prevention and treatment of ischemic stroke. In this review, we discuss the role of pro-inflammatory and anti-inflammatory mediators and related immune cells in the pathogenesis of ischemic stroke.

Association between serum cystatin C levels and the severity or potential risk factors of acute ischemic stroke

“…4 The pathogenesis of ischemic stroke is a complex combination of environmental factors, genetic factors, and a disparate assortment of various risk factors. [5][6][7][8][9] For example, clinical studies show that atherosclerosis is closely associated with the development of stroke. [10][11][12] Individuals with risk factors for atherosclerosis, such as hypertension, hypercholesterolemia, and obesity, more often develop ischemic stroke.…”

Discussion on rationality of administration of Angong Niuhuang Pills from pharmacological and toxicological perspectives

“…The mechanism of cerebral ischemia is complex, involving multiple aspects of pathology and physiology, such as excitatory amino acid toxicity, apoptosis, oxidative stress, intracellular calcium overload etc. [8] In the midst of them, inflammatory reaction is the most important damage mechanism [9]. TNFα and IL-1β play important roles in this process as two important inflammatory factors.…”

Rosmarinic acid prevents against memory deficits in ischemic mice

“…A blood flow less than 20% leads to a loss of axons and dendrites in minutes (HOFMEIJER, VAN PUTTEN, 2012;MURPHY et al, 2009). Moreover, inflammation plays a significant role in the pathogenesis of ischemic stroke (PEI et al, 2015). The inflammation responses after brain ischemia include astrocyte and microglial activation, followed by peripheral inflammatory cell infiltration in the core and penumbra zone of ischemia (GU et al, 2014;SHICHITA et al, 2014).…”