De los Reyes Lina María, Céspedes Ángel Enrique
Grupo de Investigación en Enfermedades Neurodegenerativas, Departamento de Salud Animal, Facultad de Medicina Veterinaria y Zootecnia, Universidad del Tolima.
Biomedica. 2014 Jul-Sep;34(3):366-78. doi: 10.1590/S0120-41572014000300007.
Stroke is the second leading cause of death and the first cause of disability in the world, with more than 85% of the cases having ischemic origin.
To evaluate in an embolism model of stroke the effect of atorvastatin and meloxicam on neurons, astrocytes and microglia. This evaluation was done administering each medication individually and in association.
Wistar rats were subjected to carotid arterial embolism and treatment with meloxicam and atorvastatin at 6, 24, 48 and 72 hours. Using immunohistochemistry, we evaluated the immunoreactivity of COX-2 protein, GFAP and OX-42 in neurons, astrocytes and microglia by densitometric and morphological studies. Data were evaluated by variance analysis and non-parametric multiple comparison.
Cerebral ischemia by arterial embolism increased significantly the reactivity of microglia and astrocytes (p<0.001), whereas it was reduced by atorvastatin, meloxicam and their association. Ischemia produced astrocytic shortening, cellular thickening, protoplasmic rupture expansions (clasmatodendrosis) and microglial morphological changes characteristic of various activity stages. In perifocal areas, immunoreactivity of COX-2 was increased and in the ischemic focus it was reduced, while meloxicam and atorvastatin significantly reduced (p<0.001) perifocal immunoreactivity, restoring the marking of cyclooxygenase in the ischemic focus.
These results suggest that the meloxicam-atorvastatin association attenuates astrocytic and microglial response in the inflammatory process after cerebral ischemia by arterial embolism, reducing neurodegeneration and restoring the morphological and functional balance of nervous tissue .
中风是全球第二大致死原因和第一大致残原因，超过85%的病例起源于缺血性。
在中风栓塞模型中评估阿托伐他汀和美洛昔康对神经元、星形胶质细胞和小胶质细胞的影响。通过单独给药和联合给药进行此项评估。
将Wistar大鼠进行颈动脉栓塞，并在6、24、48和72小时用美洛昔康和阿托伐他汀治疗。使用免疫组织化学，通过密度测定和形态学研究评估神经元、星形胶质细胞和小胶质细胞中COX - 2蛋白、GFAP和OX - 42的免疫反应性。数据通过方差分析和非参数多重比较进行评估。
动脉栓塞引起的脑缺血显著增加了小胶质细胞和星形胶质细胞的反应性（p<0.001），而阿托伐他汀、美洛昔康及其联合用药可使其降低。缺血导致星形胶质细胞缩短、细胞增厚、原生质破裂扩张（轴突断裂）以及小胶质细胞形态发生各种活动阶段特有的变化。在病灶周围区域，COX - 2的免疫反应性增加，而在缺血灶中则降低，而美洛昔康和阿托伐他汀显著降低（p<0.001）病灶周围的免疫反应性，恢复缺血灶中环氧化酶的标记。
这些结果表明，美洛昔康 - 阿托伐他汀联合用药可减轻动脉栓塞性脑缺血后炎症过程中的星形胶质细胞和小胶质细胞反应，减少神经变性并恢复神经组织的形态和功能平衡。
