The Effect Of COX-2 On Temporary Focal Ischemia Of Diabetes Rats

Stroke remains a major cause of mortaility and morbidity in the world. Previous studies indicated that DM is an independent risk factor for stroke,DM is strongly related to early stroke progression and associated with poorer stroke outcome. Transient ischemis, whether global or focal, is assocated with geater neuropathologic damage in DM hyperglycemic animals, and dffect prognosis. Ceebral ischemia is a pathophysiological condition indued by the oclosion of cerebral vessels by a thrombus. The resultant deprovation of blood flow, and hence Bioenergetic failure, in the ischemic braom area ev entually leds to cell deth (necrosis and apoptosis),inflammation, and tissue repair and remodeling, The inflammatory reaponse to brain ischemia has been studied extensively.Now, it is belived that diabetes could make the inflammatory of ischemia seriously. COX is the enzyme that catalyzes the first two steps in the biosynthesis of the prostaglandings from the substracts arachidonic acid(AA). Now , people clssigy cox into two isoforms:COX-l and COX-2. COX-2 is associated withinflammation but not with the physiological synthesis of PGS, it acts in a very important rule in inflammation. The pruposs is to inrestigate the role of COX-2 after temporary focal ischemia in diabetes rats.Meterials and MethodsA total of 24 healthy male 80 rat weithting 250-300g, randomly divided into 4 groups; each 6rats. Diabetes mellitus rat model is induced by STZ which wa injected into the abdomens. Temporary focal cerebral ischemia was indeced using intralluminal filament occlusion of middle cerebral artry introduced by Zea Longa. After ischemia 24h, animals were deeply anesthetized with 10%chloral Hydrate and perfused by intracadiac puncture using 4% poly-formaldehyde-0.lPBS (PH7.4). Brain were then excused and postfixted for 24h Brain tissues were embedded in paraffin, coronally sectioned(6 μ m).Immunnnohistochemistry(wabc)was used to obsrve the expression of COX-2 protein. Immunohistochemical cells are caaculated under microscope.Comparation between two groups were made using t test.All values were stated as menu眘.D.ResultImmunohistochemistry of COX-2 protein: no COX-2 immunoreactive signal was detected in non-operation groups. The number of immunoreactive cell of diabetes mellitus ischemia group is more than that of normal ischemia group.ConclussionUpregulation of COX-2 in diabetes mellitus may be relate with methaniism of diabetes mellitus aggravating cerebral infarction.