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Published on: June 18, 2021
The role of immune inflammation in aneurysmal subarachnoid hemorrhage
Zeyu Zhang1, Yuanjian Fang1, Cameron Lenahan2
1Department of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease, which mainly caused by the rupture of an intracranial aneurysm. Clinical trials have demonstrated that cerebral vasospasm (CVS) is not the sole contributor to delayed cerebral ischemia (DCI) and poor outcomes in patients with aSAH. Currently, accumulating evidence suggests that early brain injury (EBI), which occurs within 72 h after the onset of aSAH, lays the foundation for subsequent pathophysiological changes and poor outcomes of patients. The pathological mechanisms of EBI mainly include increased intracranial pressure, oxidative stress, neuroinflammation, blood-brain barrier (BBB) disruption, cerebral edema and cell death. Among them, the brain immune inflammatory responses involve a variety of immune cells and active substances, which play an important role in EBI after aSAH and may be related to DCI and long-term outcomes. Thus, attention should be paid to strategies targeting cerebral immune inflammatory responses. In this review, we discuss the role of immune inflammatory responses in the occurrence and development of aSAH, as well as some inflammatory biomarkers related to CVS, DCI, and aSAH outcomes. In addition, we also summarize the potential therapeutic drugs that target cerebral immune inflammatory responses for patients with aSAH in current research.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease, which mainly caused by the rupture of an intracranial aneurysm. Clinical trials have demonstrated that cerebral vasospasm (CVS) is not the sole contributor to delayed cerebral ischemia (DCI) and poor outcomes in patients with aSAH. Currently, accumulating evidence suggests that early brain injury (EBI), which occurs within 72 h after the onset of aSAH, lays the foundation for subsequent pathophysiological changes and poor outcomes of patients. The pathological mechanisms of EBI mainly include increased intracranial pressure, oxidative stress, neuroinflammation, blood-brain barrier (BBB) disruption, cerebral edema and cell death. Among them, the brain immune inflammatory responses involve a variety of immune cells and active substances, which play an important role in EBI after aSAH and may be related to DCI and long-term outcomes. Thus, attention should be paid to strategies targeting cerebral immune inflammatory responses. In this review, we discuss the role of immune inflammatory responses in the occurrence and development of aSAH, as well as some inflammatory biomarkers related to CVS, DCI, and aSAH outcomes. In addition, we also summarize the potential therapeutic drugs that target cerebral immune inflammatory responses for patients with aSAH in current research.
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