Laboratorio de Glicobiología, Facultad de Ciencias Médicas y Biológicas, Dr. Ignacio Chávez, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, México.
Laboratorio de Glicobiología, Facultad de Ciencias Médicas y Biológicas, Dr. Ignacio Chávez, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, México.
Arch Med Res. 2021 Jul;52(5):505-513. doi: 10.1016/j.arcmed.2021.01.009. Epub 2021 Feb 6.
Global cerebral ischemia (GCI) elicits damages to cerebral structures, learning dysfunction, memory impairments, hyperactivity, and anxiety. Circulating levels of galectin-3 (Gal-3) are associated with patient severity and outcome.
To report circulating levels of Gal-3, and cytokines (TNF-α, IL-6, IL-10) in the initial hours (acute) following GCI in a four-vessel occlusion (4-VO) rat model and the effect of melatonin treatment.
4-VO model was used to produce GCI using male Sprague-Dawley rats. Groups were: Sham-Veh, Sham-Mel, Isch-Veh and Isch-Mel. Melatonin was administered 30 min after carotid clamp removal. Gal-3 and cytokines levels were measured at 0, 30 min, 6 h and 24 h after the end of cerebral flow interruption using ELISA kits. Motor activity and anxiety were measured using open-field test.
Acute GCI (AGCI) followed by reperfusion decreased serum concentrations of TNF-α and increased IL-6 levels 24 h after ischemia, whereas melatonin reduced significantly the concentrations of these cytokines. In all groups IL-10 was higher 30 min and negligible at other times. Circulating levels of Gal-3 were reduced 30 min after ischemia/reperfusion. In the Isch-Mel group the neuroprotective effect generated a reduction in circulating Gal-3 at 6 and 24 h after AGCI, compared with all the groups. Motor activity was increased due to ischemic reperfusion, but acute melatonin treatment reduced locomotion, similar to the control group. Anxiety was reduced in the melatonin group.
Melatonin treatment following AGCI reduces pro-inflammatory factors, Gal-3, motility, and anxiety, therefore it should be considered as supplementary treatment following ischemic stroke.
全脑缺血（GCI）会导致脑结构损伤、学习功能障碍、记忆损伤、多动和焦虑。循环中的半乳糖凝集素-3（Gal-3）水平与患者的严重程度和预后相关。
报告在四血管闭塞（4-VO）大鼠模型中，GCI 后最初几小时（急性期）循环中的 Gal-3 和细胞因子（TNF-α、IL-6、IL-10）水平，以及褪黑素治疗的效果。
使用雄性 Sprague-Dawley 大鼠建立 4-VO 模型产生 GCI。组分为：假手术-vehicle（Sham-Veh）、假手术-褪黑素（Sham-Mel）、缺血-vehicle（Isch-Veh）和缺血-褪黑素（Isch-Mel）。在夹闭颈动脉后 30 分钟给予褪黑素。使用 ELISA 试剂盒在脑血流中断结束后 0、30 分钟、6 小时和 24 小时测量 Gal-3 和细胞因子水平。使用旷场试验测量运动活动和焦虑。
急性全脑缺血（AGCI）后再灌注导致血清 TNF-α浓度降低，IL-6 水平在缺血后 24 小时升高，而褪黑素显著降低这些细胞因子的浓度。在所有组中，IL-10 在 30 分钟时较高，而在其他时间则微不足道。缺血/再灌注后循环中的 Gal-3 水平降低。在 Isch-Mel 组中，与所有组相比，AGCI 后 6 小时和 24 小时，神经保护作用导致循环中的 Gal-3 减少。缺血再灌注导致运动活动增加，但急性褪黑素治疗减少了运动，与对照组相似。褪黑素组的焦虑减轻。
AGCI 后褪黑素治疗可降低促炎因子、Gal-3、运动能力和焦虑，因此应考虑作为缺血性中风后的辅助治疗。
