Abstract
To evaluate histopathological and ultrastructural changes and expression of proteins related to apoptosis CASPASE 3 and XIAP after experimental induction of temporary focal cerebral ischemia (90 minutes) due to obstruction of the middle cerebral artery in alcoholism model. Forty adult Wistar rats were used, subdivided into 5 experimental groups: control group (C); Sham group (S); Ischemic group (I); Alcoholic group (A); and Ischemic and Alcoholized group (I+A): animals submitted to the same treatment of group A and after four weeks were submitted to focal cerebral ischemia during 90 minutes, followed by reperfusion of 48 hours. Were processed for histopathological analysis and immunohistochemistry (for the protein expression of CASPASE -3 and XIAP). Greater histopathological changes were observed in the animals of groups I and I+A in the three areas analyzed. The neuronal loss was higher in the medial striatum region of the animals of groups I and I + A. The protein expression of CASPASE -3 was higher than that of XIAP in the groups I and I + A for both proteins. The expression of XIAP was slightly higher where the histopathological changes and expression of CASPASE -3 was less evident.
Highlights
Cerebral ischemia is one of the most threatening diseases in humanity with high mortality and morbidity rates worldwide[1,2]
Researches and studies performed on trial animals as well as on men concluded that excessive alcohol consumption harms the Central Nervous System[6]
Morphological and immunohistochemical analysis of proteins CASPASE 3 and XIAP in rats subjected to cerebral ischemia and chronic alcoholism Schiavoni VS et al In the striatum, diffuse interstitial edema was less evident in its lateral region
Summary
Cerebral ischemia is one of the most threatening diseases in humanity with high mortality and morbidity rates worldwide[1,2]. This is a frequent condition in clinical practice which has a difficult therapeutic solution, because the physiopathological study, among other factors, is more difficult due to the great diversity in its anatomical location, etiology and clinical manifestations[3,4,5]. Several studies have described neuronal death a few days after transient cerebral ischemia[11,12]. It remains controversial whether apoptosis or necrosis are involved in late neuronal death. By the Tunel technique, labeled cells were detected 6-24 hours after reperfusion, suggesting the existence of a time dependent evolution from the characterization of the ischemic lesion, by the close correlation observed between the activation of caspase as enzyme and the associated increase in immunoreactive product (CASPASE 3) several hours later, through the morphological and biochemical characteristics of apoptosis
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