The relationship among HS, neuroinflammation and MMP-9 in BBB injury following ischemic stroke.

Int Immunopharmacol

Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China. Electronic address:

Published: December 2024

AI Article Synopsis

  • The blood-brain barrier (BBB) plays a crucial role in maintaining the central nervous system's environment and can be damaged by CNS diseases such as ischemic stroke, leading to worse outcomes.
  • Excessive neuroinflammation after a stroke, triggered by the need to repair damaged tissue, contributes to BBB breakdown and neuronal injury, partly due to the action of matrix metalloproteinases (MMPs).
  • Hydrogen sulfide (HS) shows promise as a neuroprotective agent against BBB damage following stroke by reducing neuroinflammation and inhibiting MMP-9, revealing potential therapeutic pathways.

Article Abstract

Blood-brain barrier (BBB) is located at the interface between the central nervous system (CNS) and the circulatory system, which maintains the microenvironmental homeostasis of the CNS. BBB damage is a result of CNS diseases, including ischemic stroke, and is a cause of CNS deterioration. Cerebral ischemia unleashes a profound inflammatory response to remove the damaged tissue in the CNS and prepare the brain for repair. However, the excessive neuroinflammation following stroke onset is associated with BBB breakdown, resulting in neuronal injury and worse neurological outcomes. Additionally, matrix metalloproteinases (MMPs) are likewise responsible for the BBB injury and participate in the pathological processes of neuroinflammation following ischemic stroke. Hydrogen sulfide (HS) is one of gaseous signaling and freely diffusing molecules. Low concentration of HS yields the neuroprotection against BBB damage following stroke. This review discussed the current knowledge about the detrimental roles of neuroinflammation and MMPs in BBB injury following ischemic stroke. Specifically, we provided an updated overview of HS in protecting against BBB injury following ischemic stroke via anti-neuroinflammation and inhibiting MMP-9.

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Source
http://dx.doi.org/10.1016/j.intimp.2024.113902DOI Listing

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