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Up-regulation of PGC-1α in neurons protects against experimental autoimmune encephalomyelitis.

FASEB J. 2019; 
Dang C, Han B, Li Q, Han R, Hao J.
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Custom DNA/RNA Oligos Experimental autoimmune encephalomyelitis induction and behavioral evaluation of neurologic deficits Experimental autoimmune encephalomyelitis (EAE) was in- duced by subcutaneously injecting a solution of myelin oligo- dendrocyte glycoprotein 35–55 peptide (200 mg; GenScript, Nanjing, China) emulsified in incomplete Freund adjuvant (Thermo Fisher Scientific) and 500 mg of inactivated Mycobacte- rium tuberculosis (Thermo Fisher Scientific) into the hind flank of C57BL/6J and TG mice. Get A Quote

摘要

Reactive oxygen species (ROS) generation and mitochondrial dysfunction are related to neuron loss in multiple sclerosis (MS). Although peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) appears to play a key role in modulating levels of mitochondrial ROS, antioxidants, and uncoupling proteins (UCPs), and PGC-1α expression is reduced in the neocortex of patients with MS, it is unclear what its role is in neurons and in the manifestation of clinical symptoms of MS. Here, we show in wild-type (WT) experimental autoimmune encephalomyelitis (EAE) mice that PGC-1α is decreased 13 d after EAE induction followed by a steady decline up to 20 d. These changes were accompanied by parallel alteration... More

关键词

EAE; ROS; neuronal apoptosis