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A serious neurosurgical emergency, subarachnoid hemorrhage (SAH) is characterized by vascular and neuropathy, as well as complex pathological mechanisms like vascular lesions, inflammatory responses, and nerve cell damage. The inflammatory response is an essential aspect of SAH's pathophysiology, causing the release of a number of inflammatory mediators and oxidative stress products like TNF-α, MCP-1, MMPs, and so on, which either directly or indirectly contribute to the development of SAH.It has recently been discovered that some antibodies against inflammatory mediators, antioxidant stress, botanicals, and traditional Chinese medicine decrease the inflammatory response of SAH. Additionally, certain biomarkers linked to inflammation may serve as a foundation for clinical diagnosis.Although these mechanisms are still not completely understood, we can explore potential therapeutic targets by studying the role of inflammatory responses and bioactive molecules in the formation of SAH. • Neuroinflammatory response triggers release of mediators, oxidative stress products, and vasoactive substances post-SAH. • Targeting inflammatory signaling pathways mitigates neuroinflammation in SAH. • Vascular regulation improves cerebral hemodynamics and neuroprotection after SAH. • Inflammation-derived bioactive molecules serve as diagnostic biomarkers for SAH.
Fu et al. (Sun,) studied this question.