Department of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center (TTUHSC), 1300 Coulter Street, Amarillo, TX, 79106, USA.
College of Sciences and Health Profession, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia.
Neuromolecular Med. 2021 Dec;23(4):471-484. doi: 10.1007/s12017-021-08647-1. Epub 2021 Feb 15.
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.
在这项研究中,我们采用严格且与临床相关的实验设计和分析标准,研究了组蛋白去乙酰化酶(HDAC)抑制剂帕比司他和恩替诺特在雄性小鼠光血栓性中风后运动功能恢复中的潜力。帕比司他是一种泛 HDAC 抑制剂,已被 FDA 批准用于治疗某些癌症,而恩替诺特则是一种处于临床研究后期的 I 类 HDAC 抑制剂。药物从中风后第 5 天至第 15 天开始每隔一天(帕比司他 3 或 10mg/kg;恩替诺特 1.7 或 5mg/kg)给药。为了模拟中风幸存者的当前标准治疗方法,即物理康复,动物从中风后第 9 天至第 41 天每天在轮子上跑步(2 小时)。预定的主要终点是在网格行走和圆筒测试中的两项自发运动行为任务中测量的运动恢复。此外,我们在整个研究过程中评估了跑步距离和速度,以及研究结束时内侧颗粒皮质(AGm)中的颗粒蛋白阳性神经元数量和梗死体积。这两项感觉运动测试都表明,在中风后,将物理运动与药物联合使用并不能显著影响小鼠的运动恢复。这伴随着 AGm 中记录的颗粒蛋白阳性神经元的微小变化和实验各组之间可比的梗死体积,而在药物治疗动物的梗死周围皮质中观察到乙酰化组蛋白 3 的剂量依赖性增加。我们的观察结果表明,在具有运动功能障碍的中风幸存者中,添加帕比司他或恩替诺特治疗并结合有限的物理康复不太可能提供治疗方法。