Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-κB/IL-6/synapsin I axis in traumatic brain injury rats.
Chung-Ching ChioHung-Jung LinYu-Feng TianYu-Chieh ChenMao-Tsun LinCheng-Hsien LinChing-Ping ChangChien-Chin HsuPublished in: Journal of neuroinflammation (2017)
TBI causes neurological deficits associated with stimulating several pro-inflammatory gene profiles but inhibiting several anti-inflammatory gene profiles of cytokines and chemokines. Exercise protects against neurological injuries via stimulating an anti-inflammatory HSP70/NF-κB/IL-6/synapsin I axis in the injured brains.
Keyphrases
- traumatic brain injury
- anti inflammatory
- signaling pathway
- heat shock protein
- high intensity
- lps induced
- genome wide
- copy number
- heat shock
- physical activity
- heat stress
- pi k akt
- severe traumatic brain injury
- oxidative stress
- nuclear factor
- resistance training
- cerebral ischemia
- inflammatory response
- immune response
- blood brain barrier