Tomas-Sanchez Constantino, Blanco-Alvarez Victor Manuel, Gonzalez-Barrios Juan Antonio, Martinez-Fong Daniel, Soto-Rodriguez Guadalupe, Brambila Eduardo, Gonzalez-Vazquez Alejandro, Aguilar-Peralta Ana Karina, Limón Daniel I, Vargas-Castro Viridiana, Cebada Jorge, Alatriste-Bueno Victorino, Leon-Chavez Bertha Alicia
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 14 sur y Av. San Claudio, 72570, Puebla, Mexico.
Facultad de Enfermería, Benemérita Universidad Autónoma de Puebla, Av 25 Pte 1304, Colonia Volcanes, Puebla, Mexico.
Heliyon. 2024 Apr 25;10(9):e30017. doi: 10.1016/j.heliyon.2024.e30017. eCollection 2024 May 15.
The transient hypoxic-ischemic attack, also known as a minor stroke, can result in long-term neurological issues such as memory loss, depression, and anxiety due to an increase in nitrosative stress. The individual or combined administration of chronic prophylactic zinc and therapeutic selenium is known to reduce nitrosative stress in the first seven days post-reperfusion and, due to an antioxidant effect, prevent cell death. Besides, zinc or selenium, individually administered, also causes antidepressant and anxiolytic effects. Therefore, this work evaluated whether combining zinc and selenium could prevent stroke-elicited cognition and behavior deficits after 30 days post-reperfusion. Accordingly, we assessed the expression of growth factors at 7 days post-reperfusion, a four-time course of memory (from 7 to 28 days post-learning test), and cell proliferation, depression, and anxiety-like behavior at 30 days post-reperfusion. Male Wistar rats with a weight between 190 and 240 g) were treated with chronic prophylactic zinc administration with a concentration of 0.2 mg/kg for 15 days before common carotid artery occlusion (10 min) and then with therapeutic selenium (6 μg/kg) for 7 days post-reperfusion. Compared with individual administrations, the administration combined of prophylactic zinc and therapeutic selenium decreased astrogliosis, increased growth factor expression, and improved cell proliferation and survival in two regions, the hippocampus, and cerebral cortex. These effects prevented memory loss, depression, and anxiety-like behaviors. In conclusion, these results demonstrate that the prophylactic zinc administration combined with therapeutic selenium can reduce the long-term sequelae caused by the transient ischemic attack. Significance statement. A minor stroke caused by a transient ischemic attack can result in psychomotor sequelae that affect not only the living conditions of patients and their families but also the economy. The incidence of these micro-events among young people has increased in the world. Nonetheless, there is no deep understanding of how this population group responds to regular treatments (Ekker and et al., 2018) [1]. On the basis that zinc and selenium have antioxidant, anti-inflammatory, and regenerative properties in stroke animal models, our work explored whether the chronic combined administration of prophylactic zinc and therapeutic selenium could prevent neurological sequelae in the long term in a stroke rat model of unilateral common carotid artery occlusion (CCAO) by 10-min. Our results showed that this combined treatment provided a long-term neuroprotective effect by decreasing astrogliosis, memory loss, anxiety, and depression-like behavior.
短暂性缺氧缺血发作,也被称为轻度中风,由于亚硝化应激增加,可能导致长期的神经问题,如记忆力丧失、抑郁和焦虑。已知长期预防性给予锌和治疗性给予硒单独或联合使用,可在再灌注后的头七天内降低亚硝化应激,并由于抗氧化作用预防细胞死亡。此外,单独给予锌或硒也会产生抗抑郁和抗焦虑作用。因此,本研究评估了锌和硒联合使用是否能预防再灌注30天后中风引发的认知和行为缺陷。相应地,我们评估了再灌注7天时生长因子的表达、学习测试后7至28天的四个记忆时间进程,以及再灌注30天时的细胞增殖、抑郁和焦虑样行为。体重在190至240克之间的雄性Wistar大鼠,在颈总动脉闭塞(10分钟)前15天,以0.2毫克/千克的浓度进行长期预防性锌给药,然后在再灌注后7天给予治疗性硒(6微克/千克)。与单独给药相比,预防性锌和治疗性硒联合给药可减少星形胶质细胞增生,增加生长因子表达,并改善海马体和大脑皮层两个区域的细胞增殖和存活。这些作用预防了记忆力丧失、抑郁和焦虑样行为。总之,这些结果表明,预防性锌给药与治疗性硒联合使用可减少短暂性缺血发作引起的长期后遗症。意义声明。短暂性缺血发作引起的轻度中风可导致精神运动后遗症,不仅影响患者及其家庭的生活状况,还影响经济。在世界范围内,这些微事件在年轻人中的发病率有所增加。尽管如此,对于这一人群对常规治疗的反应仍缺乏深入了解(埃克等人,2018年)[1]。基于锌和硒在中风动物模型中具有抗氧化、抗炎和再生特性,我们的研究探讨了长期联合预防性锌和治疗性硒给药是否能在单侧颈总动脉闭塞(CCAO)10分钟的中风大鼠模型中长期预防神经后遗症。我们的结果表明,这种联合治疗通过减少星形胶质细胞增生、记忆力丧失、焦虑和抑郁样行为,提供了长期的神经保护作用。