ArticleBehavioural neurology2018
Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury via ERK Signaling.
Article in Behavioural neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- MAM-mediated mitophagy and endoplasmic reticulum stress: the hidden regulators of ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Dl-3-n-butylphthalide promotes angiogenesis in ischemic stroke mice through upregulating autocrine and paracrine sonic hedgehog.Acta pharmacologica Sinica · 2023Article
- Tetramethylpyrazine ameliorates endotoxin-induced acute lung injury by relieving Golgi stress via the Nrf2/HO-1 signaling pathway.BMC pulmonary medicine · 2023Article
- Dl-butylphthalide inhibits rotenone-induced oxidative stress in microglia via regulation of the Keap1/Nrf2/HO-1 signaling pathway.Experimental and therapeutic medicine · 2021Article
- The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- PAQR3 protects against oxygen-glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells.Journal of molecular histology · 2020Article
- Neuroprotective mechanisms of 3-n-butylphthalide in neurodegenerative diseases.Biomedical reports · 2019Article
- Application and prospects of butylphthalide for the treatment of neurologic diseases.Chinese medical journal · 2019Review
- Article
- Role of the Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway in Ischemia-Reperfusion Injury.Frontiers in physiology · 2019Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe aim of this study was to explore the role of DL-3-n-butylphthalide (NBP) in cerebral ischemia-reperfusion injury (CIRI) mice model. The involvement of extracellular signal-regulated kinase (ERK) signaling pathway was also investigated.
methodsAll mice were divided into five groups: sham-operated group, CIRI group, NBP pretreatment group, NBP treatment group, and NBP pretreatment + treatment group. The CIRI mice model was established by the use of the Pulsinelli four-vessel occlusion method. Pretreatment mice received NBP (90 mg/kg/d) three times a day within four days before reperfusion by gavage. Treatment mice received NBP (90 mg/kg/d) three times a day within five days after reperfusion by gavage. We detected the infarction area, the neurological severity, and the superoxide dismutase and malondialdehyde levels. Furthermore, we observed the expressions of GRASP65, phosphorylation of GRASP65 (pGRASP65), ERK, and phosphorylation of ERK (pERK) by the use of Western blotting.
resultsThe result showed that the ERK pathway was activated in response to CIRI. NBP decreases the expressions of pERK and pGRASP65 following CIRI. Additionally, NBP could decrease MDA and increase SOD level in brain tissues. Decreased infarct volume was also observed in the NBP group. Thereby, NBP inhibited the activation of the ERK pathway induced by CIRI and reduced the GRASP65 phosphorylation.
conclusionsThe current finding suggested that NBP protected the cerebrum from CIRI mediated by inhibiting the ERK signaling pathway and subsequently reducing GRASP65 phosphorylation.
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