Impact of inflammation on brain subcellular energetics in anesthetized rats.
Robert H ThieleHari P OsuruUmadevi PailaKeita IkedaZhiyi ZuoPublished in: BMC neuroscience (2019)
In the setting of inflammation, rats exposed to isoflurane show increased hypoxia-inducible factor-1α expression despite a lack of hypoxia, increased oxidative stress in the brain, and increased serum lactate, all of which suggest a relative increase in anaerobic metabolism compared to propofol. Differences in oxidative stress as well as heat shock protein 90 and NF-κβ inhibitor may account for the differential expression of cerebral hypoxia-inducible factor-1α during inflammation.
Keyphrases
- oxidative stress
- heat shock protein
- diabetic rats
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- resting state
- heat shock
- white matter
- cerebral ischemia
- poor prognosis
- microbial community
- wastewater treatment
- functional connectivity
- signaling pathway
- endothelial cells
- binding protein
- brain injury
- multiple sclerosis
- endoplasmic reticulum stress
- anaerobic digestion