ArticleNeural regeneration research2020
Neuroprotective mechanism of TMP269, a selective class IIA histone deacetylase inhibitor, after cerebral ischemia/reperfusion injury.
Article in Neural regeneration research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- β-hydroxybutyrate restores social deficits by suppressing HDAC9 in the ACC of Shank3B-deficient mice.EMBO molecular medicine · 2026Article
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- Carrier-Free Nanocapsule with Dual-Target Capacity for Synergistically Restoring Inflammatory Microenvironment and Microbiota Dysbiosis in Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HDAC9 Deficiency Upregulates cGMP-dependent Kinase II to Mitigate Neuronal Apoptosis in Ischemic Stroke.Translational stroke research · 2025Article
- Class IIa histone deacetylase (HDAC) inhibitor TMP269 suppresses lumpy skin disease virus replication by regulating host lysophosphatidic acid metabolism.Journal of virology · 2025Article
- A General Amino-(Hetero)arylation of Simple Olefins with (Hetero)aryl Sulfonamides Enabled by anACS catalysis · 2025Article
- Epigenetic drug screening identifies enzyme inhibitors A-196 and TMP-269 as novel regulators of sprouting angiogenesis.Scientific reports · 2025Article
- Cerebral Inhibition of the H3K9 Methylation Could Ameliorate Blood-Brain Barrier Dysfunction and Neural Damage in Vascular Dementia.Archives of Razi Institute · 2024Article
- BML-281 promotes neuronal differentiation by modulating Wnt/CaMolecular and cellular biochemistry · 2024Article
- A novel histone deacetylase inhibitor W2A-16 improves the barrier integrity in brain vascular endothelial cells.Frontiers in cellular neuroscience · 2024Article
- TMP269, a small molecule inhibitor of class IIa HDAC, suppresses RABV replicationFrontiers in microbiology · 2023Article
- HDAC1 is Involved in Neuroinflammation and Blood-Brain Barrier Damage in Stroke Pathogenesis.Journal of inflammation research · 2023Article
- Stroke by inducing HDAC9-dependent deacetylation of HIF-1 and Sp1, promotes TfR1 transcription and GPX4 reduction, thus determining ferroptotic neuronal death.International journal of biological sciences · 2023Article
- Blood-Brain Barrier Disintegration in Growth-Restricted Fetuses with Brain Sparing Effect.International journal of molecular sciences · 2022Article
- Epigenetics in blood-brain barrier disruption.Fluids and barriers of the CNS · 2021Review
- Gestational Hypoxia and Blood-Brain Barrier Permeability: Early Origins of Cerebrovascular Dysfunction Induced by Epigenetic Mechanisms.Frontiers in physiology · 2021Review
- 4-Phenylbutyrate ameliorates apoptotic neural cell death in Down syndrome by reducing protein aggregates.Scientific reports · 2020Article
- Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke.Disease markers · 2020Review
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6 authors.
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Abstract
TMP269 is a selective class IIA histone deacetylase inhibitor that has a protective effect on the central nervous system, whose specific mechanism of action is unclear. We aimed to reveal the optimal concentration of TMP269 for protecting against cerebral ischemia/reperfusion injury and its neuroprotective mechanism. Male Sprague-Dawley rats were randomly divided into sham, ischemia/reperfusion, and 1, 4, 10 and 16 mg/kg TMP269 groups. Cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion. TMP269 was intraperitoneally administered at different doses 0.5 hours before ischemia induction. Western blot assay and immunohistochemistry were used to detect effects of TMP269 on histone 2 acetylation. The results showed that the level of histone 2 acetylation was increased 24 hours after TMP269 injection. 2,3,5-Triphenyltetrazolium chloride staining was utilized to examine effect of TMP269 on infarct volume. The results found that different doses of TMP269 could reduce the infarct volume. Western blot assay, immunohistochemistry and Evans blue staining were employed to measure the effect of TMP269 on blood-brain barrier. The results showed that TMP269 counteracted the abnormal endothelial cell permeability changes caused by cerebral ischemia/reperfusion. Western blot assay and immunohistochemistry were used to determine the effect of TMP269 on tissue kallikrein. The results found that TMP269 up-regulated the expression of tissue kallikrein. Western blot assay further determined the optimal concentration to be 4 mg/kg. In conclusion, TMP269 plays a neuroprotective role by up-regulating the level of histone 2 acetylation, alleviating endothelial cell injury after cerebral ischemia/reperfusion, and up-regulating the expression of tissue kallikrein. The experimental protocol was approved in 2014 by the Department of Laboratory Animal Science, Fudan University, China (approval No. 20140143C001).
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