Archives of medical research · 2017
Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat.
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Cetin Cansel, Erdogan Ahmet Melih, Dincel Gungor Cagdas, Bakar Bulent, Kisa Ucler
Аннотация
BACKGROUND: Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.
AIMS OF THE STUDY: Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
AIMS OF THE STUDY: Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.