ArticleJournal of molecular neuroscience : MN2015
Probucol Protects Against Asymmetric Dimethylarginine-Induced Apoptosis in the Cultured Human Brain Microvascular Endothelial Cells.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- The therapeutic potential of probucol and probucol analogues in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Asymmetric dimethylarginine induces maladaptive function of the blood-brain barrier.Frontiers in cell and developmental biology · 2024Article
- Protective Effects of Probucol on Different Brain Cells Exposed to Manganese.Neurotoxicity research · 2022Article
- Probucol Prevents Diabetes-Induced Retinal Neuronal Degeneration through Upregulating Nrf2.BioMed research international · 2020Article
- Tissue Plasminogen Activator Causes Brain Microvascular Endothelial Cell Injury After Oxygen Glucose Deprivation by Inhibiting Sonic Hedgehog Signaling.Neurochemical research · 2019Article
- Brain-derived neurotrophic factor secreted by the cerebral endothelium: A new actor of brain function?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Effect of probucol on hemodynamics, rheology and blood lipid of diabetic retinopathy.Experimental and therapeutic medicine · 2018Article
- Antidepressant Effects of Probucol on Early-Symptomatic YAC128 Transgenic Mice for Huntington's Disease.Neural plasticity · 2018Article
- Asymmetric dimethylarginine downregulates sarco/endoplasmic reticulum calcium‑ATPase 3 and induces endoplasmic reticulum stress in human umbilical vein endothelial cells.Molecular medicine reports · 2017Article
- Regulation of c-Jun N-Terminal Protein Kinase (JNK) Pathway in Apoptosis of Endothelial Outgrowth Cells Induced by Asymmetric Dimethylarginine.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- The Cerebral Brain-Derived Neurotrophic Factor Pathway, Either Neuronal or Endothelial, Is Impaired in Rats with Adjuvant-Induced Arthritis. Connection with Endothelial Dysfunction.Frontiers in physiology · 2017Article
- Activation of sonic hedgehog signaling attenuates oxidized low-density lipoprotein-stimulated brain microvascular endothelial cells dysfunction in vitro.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Asymmetric dimethylarginine (ADMA) is emerging as a key contributor to endothelial dysfunction. The drug probucol was reported to have an anti-lipid peroxidation effect and improve endothelial dilation function. But little is known about the protective effect of probucol on ADMA-induced human brain microvascular endothelial cell (HBMEC) injury and its underlying mechanisms. Therefore, in this study, we investigated the effect of probucol on ADMA-induced HBMEC injury and its potential mechanisms. Results showed that probucol protected against ADMA-induced HBMEC injury in a dose-dependent manner; probucol pretreatment also significantly reduced the level of reactive oxygen species (ROS) and malondialdehyde (MDA), downregulated the expression of pro-apoptotic gene Bax and caspase-3 activity, as well as increased the brain-derived neurotrophic factor (BDNF) release and promoted anti-apoptotic gene Bcl-2 and eNOS expression in the cultured HBMECs. Furthermore, we found that ADMA significantly increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and p38, while probucol pretreatment effectively inhibited ADMA-induced JNK and p38 phosphorylation in HBMECs. In conclusion, our present results demonstrated that probucol protected against ADMA-induced HBMEC injury and suppressed oxidative stress through the JNK/p38 MAPK pathway, which was the potential underlying mechanism of HBMEC injury in ischemic cerebrovascular disease.
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