Overall, our findings demonstrate that RGFP966 can mitigate the first brain damage and neurological impairments in TBI. The underlying mechanism involves triggering the Nrf2-mediated AO system and negatively regulating the HMGB1/TLR4-mediated NLRP3 inflammasome pathway.
Keyphrases
- oxidative stress
- nlrp inflammasome
- histone deacetylase
- resting state
- diabetic rats
- white matter
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- cerebral ischemia
- traumatic brain injury
- spinal cord injury
- functional connectivity
- toll like receptor
- inflammatory response
- signaling pathway
- immune response
- multiple sclerosis
- brain injury
- heat shock protein