Cetin Cansel, Erdogan Ahmet Melih, Dincel Gungor Cagdas, Bakar Bulent, Kisa Ucler
Kirikkale University, Faculty of Medicine, Kirikkale, Turkey.
Aksaray University, Eskil Vocational High Scool, Laboratory and Veterinary Science, Aksaray, Turkey.
Arch Med Res. 2017 Apr;48(3):247-256. doi: 10.1016/j.arcmed.2017.06.004.
Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.
Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically.
Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1β, IL-6, MPO, NO, and TNFα levels. It could increase IL-1β levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels.
Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.
目前,脑缺血/再灌注(I/R)损伤的管理仍然是一个困难的过程。
本研究旨在探讨柳氮磺胺吡啶对大鼠脑短暂性I/R损伤的治疗特性。
除对照组(n = 5)外,将20只Wistar白化大鼠分配用于I/R损伤的急性期和慢性期研究,并尝试对双侧颈内动脉夹闭临时动脉瘤夹30分钟。4小时后,对SL-A组和SL-C组的动物每天口服一次40mg/kg柳氮磺胺吡啶。将动物断头,然后通过组织病理学计数或评估固缩和坏死的神经元细胞、血管周围水肿、海马区细胞间组织不规则(IIO)以及顶叶皮质坏死神经元。对组织丙二醛(MDA)、髓过氧化物酶(MPO)、总亚硝酸盐/硝酸盐(NO)、白细胞介素1-β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平值进行生化评估。
柳氮磺胺吡啶在两个阶段均可减轻血管周围水肿、IIO、皮质和海马神经元细胞死亡。它在急性期可降低MDA,但不能降低IL-1β、IL-6、MPO、NO和TNFα水平。它在慢性期可增加IL-1β水平,但不影响IL-6、MPO、MDA、NO、TNF-α水平。
柳氮磺胺吡啶可改善大鼠I/R损伤两个阶段缺氧组织的组织病理学结构。它仅在急性期抑制脂质过氧化级联反应。这些结果表明,未来的研究应使用更具体的实验室方法来研究柳氮磺胺吡啶在脑I/R损伤中的治疗机制。