Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis.
In conclusion, these data implied that excessive mitochondrial fission might inhibit mitochondrial complex I to become a cause of oxidative stress in SAH, and the inhibition of Drp1 by Mdivi-1 attenuated early brain injury after SAH probably via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis.
PMID: 28790012 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - Category: Biology Authors: Fan LF, He PY, Peng YC, Du QH, Ma YJ, Jin JX, Xu HZ, Li JR, Wang ZJ, Cao SL, Li T, Yan F, Gu C, Wang L, Chen G Tags: Free Radic Biol Med Source Type: research
More News: Alzheimer's | Biology | Brain | Hemorrhagic Stroke | Huntington's Disease | Mitochondria | Mitochondrial Disease | Molecular Biology | Neurology | Parkinson's Disease | Study | Subarachnoid Hemorrhage | Translocation