Abstract
Subarachnoid hemorrhage (SAH) has a high mortality rate and causes long-term disability in many patients, often associated with cognitive impairment. However, the pathogenesis of delayed brain dysfunction after SAH is not fully understood. A growing body of evidence suggests that neuroinflammation and oxidative stress play a negative role in neurofunctional deficits. Red blood cells and hemoglobin, immune cells, proinflammatory cytokines, and peroxidases are directly or indirectly involved in the regulation of neuroinflammation and oxidative stress in the central nervous system after SAH. This review explores the role of various cellular and acellular components in secondary inflammation and oxidative stress after SAH, and aims to provide new ideas for clinical treatment to improve the prognosis of SAH.
Highlights
Six to nine in 100,000 people seek medical attention for subarachnoid hemorrhage (SAH) annually
This review explores the role of various cellular and acellular components in secondary inflammation and oxidative stress after SAH, and aims to provide new ideas for clinical treatment to improve the prognosis of SAH
Many studies have shown that inflammatory response and oxidative stress play an important role in the progression and prognosis of SAH
Summary
Six to nine in 100,000 people seek medical attention for subarachnoid hemorrhage (SAH) annually. SAH accounts for only 5% of all strokes, it imposes a significant health burden on society due to its young age of onset Those who survive the initial bleeding often develop severe disability, with cognitive impairment, known as delayed ischemic neurological deficit (DIND) (Macdonald, 2014). Nimodipine may reduce the incidence of DCI and the risk of poor prognosis after SAH by preventing and reducing vasospasm through muscle wall relaxation. TLR-4 plays a major role in the inflammatory response after SAH (Okada and Suzuki, 2017). TLR4-dependent proinflammatory cytokines trigger an inflammatory response similar to that induced by lipopolysaccharide (Grylls et al, 2021). TRAF6 is associated with transforming factor-β-activated kinase (TAK), which leads to activation of the NF-κB signaling pathway and increased transcription and expression of proinflammatory cytokines (Karimy et al, 2020). The two different connective proteins act in different ways, both activate the NF-κB signaling pathway and trigger further inflammatory cascades (Takeuchi and Akira, 2010)
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