| Literature DB >> 33590407 |
Abdullah Al Shoyaib1, Faisal F Alamri1,2,3, Nausheen Syeara1, Srinidhi Jayaraman1, Serob T Karamyan4, Thiruma V Arumugam5, Vardan T Karamyan6,7.
Abstract
Using rigorous and clinically relevant experimental design and analysis standards, in this study, we investigated the potential of histone deacetylase (HDAC) inhibitors panobinostat and entinostat to enhance recovery of motor function after photothrombotic stroke in male mice. Panobinostat, a pan-HDAC inhibitor, is a FDA-approved drug for certain cancers, whereas entinostat is a class-I HDAC inhibitor in late stage of clinical investigation. The drugs were administered every other day (panobinostat-3 or 10 mg/kg; entinostat-1.7 or 5 mg/kg) starting from day 5 to 15 after stroke. To imitate the current standard of care in stroke survivors, i.e., physical rehabilitation, the animals run on wheels (2 h daily) from post-stroke day 9 to 41. The predetermined primary end point was motor recovery measured in two tasks of spontaneous motor behaviors in grid-walking and cylinder tests. In addition, we evaluated the running distance and speed throughout the study, and the number of parvalbumin-positive neurons in medial agranular cortex (AGm) and infarct volumes at the end of the study. Both sensorimotor tests revealed that combination of physical exercise with either drug did not substantially affect motor recovery in mice after stroke. This was accompanied by negligible changes of parvalbumin-positive neurons recorded in AGm and comparable infarct volumes among experimental groups, while dose-dependent increase in acetylated histone 3 was observed in peri-infarct cortex of drug-treated animals. Our observations suggest that add-on panobinostat or entinostat therapy coupled with limited physical rehabilitation is unlikely to offer therapeutic modality for stroke survivors who have motor dysfunction.Entities:
Keywords: Drug repurposing; HDAC inhibitor; Neural repair; Post-stroke recovery; Pre-clinical trial; Stroke pharmacotherapy
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Year: 2021 PMID: 33590407 PMCID: PMC8364572 DOI: 10.1007/s12017-021-08647-1
Source DB: PubMed Journal: Neuromolecular Med ISSN: 1535-1084 Impact factor: 3.843