Attenuation of cerebral ischemia–reperfusion injury by exogenous hydrogen sulphide: involvement of the Nrf2/HO-1 pathway in NLRP3 inflammasome inhibition

Key Points

• To explore how exogenous hydrogen sulphide (H₂S) can protect the brain from ischemia-reperfusion injury and the underlying mechanisms involved.
• Administration of exogenous hydrogen sulphide in a controlled experimental setup.
• Assessment of the Nrf2/HO-1 antioxidant pathway during treatment.
• Evaluation of NLRP3 inflammasome activation levels post-treatment.
• Exogenous H₂S significantly reduced cerebral ischemia-reperfusion injury.
• Activation of the Nrf2/HO-1 pathway was notably enhanced with H₂S treatment.
• Inhibition of NLRP3 inflammasome activation was effectively achieved with exogenous H₂S.

Abstract