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Suppression of mitochondrial fission in experimental cerebral ischemia: The potential neuroprotective target of p38 MAPK inhibition.

Abstract：

:In the present study, we investigated the neuroprotective role of p38 inhibition on experimental stroke in rats. p38 inhibition treatment alleviated the brain infarction volume and neurological deficits following ischemia, promoted the activation of Extracellular signal-regulated kinases (ERK1/2), suppressed the activation of Glycogen synthase kinase 3 beta (GSK3b). Application of two p38 inhibitors, both SB239063 and Losmapimod could down-regulate DLP1 and MFF, which were involved in mitochondrial fission and fragmentation. Losmapimod application progressively suppressed DLP1/MFF from 6 h to 24 h after ischemia-reperfusion injury. SB239063 pretreatment further showed the suppression of DLP1/MFF, and up-regulated the protein levels of p62 and Mitochondrial Complex I at 5 mg/kg dose. Our results suggested that inhibition of p38 MAPK attenuated mitochondrial fragmentation/mitophagy after ischemic attack. In conclusion, p38 inhibition treatment might promote cellular survival signaling pathways, attenuate mitochondrial autophagy to maintain mitochondrial contents. This study suggests a potential neuroprotective target of p38 inhibition via suppressing mitochondrial fragmentation/mitophagy in cerebral ischemic injury.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Zhang XM,Zhang L,Wang G,Niu W,He Z,Ding L,Jia J

doi

10.1016/j.neuint.2015.06.010

subject

Has Abstract

pub_date

2015-11-01 00:00:00

pages

1-8

eissn

0197-0186

issn

1872-9754

pii

S0197-0186(15)00094-7

journal_volume

90

pub_type

杂志文章

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