| IntroductionStoke remains a major cause of mortality and morbidity in the world. Previous studies indicated that diabetes mellitus ( DM) is an independent risk factor for stroke. , DM is strongly related to early stroke progression and associated with poorer stroke outcome. Transient ischemia, whether global or focal, is associated with greater neu-ropathologic damage in DM hyperglycemic animals, and effect prognosis. Cerebral ischemia is a pathophysiological condition induced by the occlusion of cerebral vessels by a thrombus. The resultant deprivation of blood flow, and hence Bioenergetic failure, in the ischemic brain area eventually leads to cell death ( necrosis and apoptosis) , inflammation, and tissue repair and remodeling. The inflammatory response to brain ischemia has been studied extensively. Accumulating evidence suggests that the acute inflammatory response after ischemic brain injury is mediated by a sequence of gene expression, including inflammatory cytokines, chemokines, cellular adhesion molecules, and other proinflammatory genes, and CD44 is one of cellular adhesion molecules. CD44 is a highly heterogeneity family of cell surface proteoglycan, represent products of a single gene and widely expressing in various tissues. Act as a major cell surface receptor for hyaluro-nan, CD44 - HA interactions plays a crucial role in inflammation re-actions. Multiple roles for CD44 in inflammation include endothelial cells recognizing, lymphocyte homing, matrix remodeling and regulation of cytokines gene expression. Infarct volume and expression of CD44 were detected by making rat model of focal cerebral ischemia induced by intxaluminal filament occlusion of middle cerebral artery. The purpose is to investigate the role of CD44 after temporary focal ischemia in diabetes mellitus rats.Meterials and MethodsA total of 32 healthy male wistar rat weighting 100 - 130g, randomly divided into 8 groups; reperfusion 1h, 3h, 6h, 12h, 24h, 48h, 72h, 7d after 2h MCAO respectively, each 4 rats. Other 5 healthy male wistar rat weighting 180 - 200g is control group for reperfusion 24h after 2h MCAO. Diabetes mellitus rat model is induced by STZ which was injected into the abdomens. Temporary focal cerebral ischemia was induced using intxaluminal filament occlusion of middle cerebral artery introduced by Zea Longa. At various times after ischemia (1h, 3h, 6h, 12h, 24h, 48h, 72h, 7d) , animals were deeply anesthetized with 10% Chloral Hydrate and perfused by intracadiac puncture using 4% poly formaldehyde -0. 1PBS ( PH 7.4). Brain were then excised and postfixted for 24h Brain tissues were embedded in paraffin, coronally sectioned ( 6um) . The size of infarct on coronal sections of HE staining were measured using pathologic image analysis system. The infarct volume was calculated as the sum of the sectional infarct areas multiplied by the interval thickness. Immunohistochemis-try ( SABC) was used to observe the expression of CD44 protein. Semi - quantitative method was applied to analysis immunohistochemi-cal cells. All values were stated as mean S. D. Comparisons between diabetes mellitus group and control group at 24 time - points of cerebral ischemia or CD44 were made using t - test. Statistical comparisons the expression of CD44 and infarction volume between diabetes mellitus groups were made by ANOVA.Result1. Infarct volume: The infarct lesion was initially found at Ih after MCAO - R within the territory of the occluded middle cerebral artery including cortex and subcortical areas with light microscope. The boundaries between areas of ischemic damage and the adjacent normal areas of the brain could be sharply delineated. The infarct volume then evolved until 24h after MCAO - R and did not significantly vary from 24h to 72h, but decreased at 7d. diabetes mellitus group increased the infarct volume significantly compared with that of control group at 24 time - points after MCAO - R.2. Immunohistochemistry of CD44 protein: no CD44 immunoreac-tive signal was detected in diabetes mellitus r... |
PDF Full Text Request