ArticleExperimental and therapeutic medicine2021
Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Potential neuroprotective and therapeutic agents and their mechanisms for irradiation-induced brain injury.Ibrain · 2026Review
- Plant polysaccharides in neuroprotection: mechanistic insights across central nervous system disorders.Frontiers in pharmacology · 2025Review
- Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling.Experimental and therapeutic medicine · 2024Article
- Anti-Glioma Effects of Ligustilide or n-Butylphthalide on Their Own and the Synergistic Effects with Temozolomide via PI3K/Akt Signaling Pathway.OncoTargets and therapy · 2023Article
- Pramipexole Inhibits Neuronal Apoptosis in Rats with Parkinson's Disease.Journal of healthcare engineering · 2022Article
- Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cerebral Ischemia/Reperfusion Injury.Frontiers in cellular neuroscience · 2022Review
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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
The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. A total of 36 Sprague-Dawley rats were randomly divided into sham-operation group (n=12), model group (n=12) and butylphthalide group (n=12). Additionally, qPCR was performed to measure the mRNA expression of Bax and Bcl-2, and a TUNEL assay was conducted to investigate the cell apoptosis. Compared with the sham-operation group, the model group and the butylphthalide group had notably increased Zea-Longa scores (P<0.05), while the butylphthalide group exhibited a markedly decreased Zea-Longa score, compared with the model group (P<0.05). The positive expression of Bax was markedly higher (P<0.05), while that of Bcl-2 was notably lower in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. Furthermore, the positive expression of Bax was notably decreased (P<0.05), while that of Bcl-2 was markedly increased in the butylphthalide group in comparison with those in model group (P<0.05). The model group and the butylphthalide group had markedly higher relative protein expression levels of p-JNK and p-p38 MAPK than the sham-operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p-JNK and p-p38 MAPK than the model group (P<0.05). The relative mRNA expression level of Bax was markedly increased (P<0.05), while that of Bcl-2 was notably decreased in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. Compared with those in the model group, the relative mRNA expression level of Bax decreased markedly (P<0.05), and that of Bcl-2 increased notably in the butylphthalide group (P<0.05). The apoptotic rate was markedly higher in the model group and the butylphthalide group than that in the sham-operation group (P<0.05), but it was notably lower in the butylphthalide group than that in the model group (P<0.05). In conclusion, butylphthalide may inhibit nerve cell apoptosis in rats with cerebral infarction to exert a protective effect, which may be associated with the JNK/p38 MAPK signaling pathway.
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