Pharmacological Modulations of Nrf2 and Therapeutic Implications in Aneurysmal Subarachnoid Hemorrhage.
Qia ZhangJianmin ZhangJun MoPublished in: Molecules (Basel, Switzerland) (2023)
An aneurysmal subarachnoid hemorrhage (aSAH) is a subtype of stroke with high morbidity and mortality. The main causes of a poor prognosis include early brain injury (EBI) and delayed vasospasm, both of which play a significant role in the pathophysiological process. As an important mechanism of EBI and delayed vasospasm, oxidative stress plays an important role in the pathogenesis of aSAH by producing reactive oxygen species (ROS) through the mitochondria, hemoglobin, or enzymatic pathways in the early stages of aSAH. As a result, antioxidant therapy, which primarily targets the Nrf2-related pathway, can be employed as a potential strategy for treating aSAH. In the early stages of aSAH development, increasing the expression of antioxidant enzymes and detoxifying enzymes can relieve oxidative stress, reduce brain damage, and improve prognosis. Herein, the regulatory mechanisms of Nrf2 and related pharmacological compounds are reviewed, and Nrf2-targeted drugs are proposed as potential treatments for aSAH.
Keyphrases
- oxidative stress
- poor prognosis
- brain injury
- subarachnoid hemorrhage
- reactive oxygen species
- cerebral ischemia
- dna damage
- long non coding rna
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- cell death
- nitric oxide
- atrial fibrillation
- heat shock
- risk assessment
- stem cells
- hydrogen peroxide
- blood brain barrier
- signaling pathway
- resting state
- cell therapy
- transcription factor
- binding protein
- functional connectivity
- endoplasmic reticulum