ArticleInternational journal of molecular medicine2018
Vitamin D receptor activation influences the ERK pathway and protects against neurological deficits and neuronal death.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Unlocking the Potential of Vitamin D: A Comprehensive Exploration of Its Role in Neurological Health and Diseases.Biology · 2025Review
- Effects of the Interaction between Dietary Vitamin DAnimals : an open access journal from MDPI · 2024Article
- Tremendous Fidelity of Vitamin D3 in Age-related Neurological Disorders.Molecular neurobiology · 2024Review
- Curcumin inhibits cerebral ischaemia-reperfusion injury and cell apoptosis in rats through the ERK-CHOP-caspase-11 pathway.Pharmaceutical biology · 2022Article
- Vitamin D3 and Ischemic Stroke: A Narrative Review.Antioxidants (Basel, Switzerland) · 2022Review
- Double-Edged Sword of Vitamin D3 Effects on Primary Neuronal Cultures in Hypoxic States.International journal of molecular sciences · 2021Article
- Benefits of vitamin D supplementation to attenuate TBI secondary injury?Translational neuroscience · 2021Review
- Article
- RNAi-mediated knockdown of VDR surprisingly suppresses cell growth in Jurkat T and U87-MG cells.Heliyon · 2019Article
- Article
- The combined presence of hypertension and vitamin D deficiency increased the probability of the occurrence of small vessel disease in China.BMC neurology · 2019Article
- Effect of β-patchoulene on cerebral ischemia-reperfusion injury and the TLR4/NF-κB signaling pathway.Experimental and therapeutic medicine · 2019Article
- The regulatory role of Toll-like receptors after ischemic stroke: neurosteroids as TLR modulators with the focus on TLR2/4.Cellular and molecular life sciences : CMLS · 2019Review
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that global cerebral ischemia (GCI) causes neurological deficits and neuronal cell apoptosis. Calcitriol, a biologically active metabolite of vitamin D, exerts its endocrinological influence via nuclear vitamin D receptor. It is being assessed as an emerging therapeutic strategy in models of various medical conditions, including acute brain injury. The purpose of the present study was to investigate the neuroprotective effects of calcitriol on GCI and further refine the potential underlying mechanisms. A total of 145 male rats were assigned to 5 groups as follows: Sham group, GCI group, calcitriol treatment group, PD98059 treatment group and vehicle-treated group. Brain water content and neurologic severity score were assessed to evaluate the brain edema and neurological deficits of rats. Histopathological changes and ultrastructures of cells were observed via hematoxylin and eosin stain and transmission electron microscopy, respectively. Immunofluorescent staining and western blot analysis were used to assess the expression of proteins and their co-localization at the molecular level. The results demonstrated that post-GCI administration of calcitriol attenuated brain edema and improved neurological function in rats. Calcitriol also caused marked extracellular signal-regulated kinase 1/2 pathway activation, and thereby attenuated neuronal apoptosis. The present study provided novel clues for understanding the mechanisms by which calcitriol exerts its neuroprotective activity in a rat model of GCI.
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