Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats
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2021, Vascular PharmacologyCitation Excerpt :BCCAo is an established and commonly used animal model to induce VaD as a consequence of cerebrovascular hypoperfusion and related abnormalities [39]. Decreased cerebral perfusion; endothelial dysfunction; impairment of learning and memory and neuropathological changes have been reported to be associated with BCCAo [54,57,58]. Impaired blood supply to brain regions during BCCAo is further known to cause severe oxidative stress [59] and produce cholinergic dysfunction [39].
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2020, Biomedicine and PharmacotherapyCitation Excerpt :Cerebral ischemia reperfusion (I/R) was performed in rats after orally treating the rats with 25 mg/kg bodyweight (b.wt) and 50 mg/kg b.wt of tomentosin daily for seven consecutive days. The cerebral occlusion was carried as per the previous protocol [32]. The rats were anesthetized with intraperitoneal injection of 1% pentobarbital sodium solution (30 mg/kg) and the skin was exposed through an incision in midline neck.
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2020, Life SciencesCitation Excerpt :The doses were chosen according to previous studies [19–23] and to our preliminary studies. After 14 days of pretreatment the first, sixth, seventh and eighth groups served as sham operated rats pretreated with vehicle, fenofibrate (100 mg/kg/day p.o) pioglitazone (10 mg/kg/day p.o) and fenofibrate (100 mg/kg/day) + pioglitazone (10 mg/kg/day) while, the other groups were subjected to ischemia reperfusion (I/R) injury as previously described [24,25]. Briefly, animals were anaesthetized by intraperitoneal injection of a mixture of ketamine (80 mg/kg) and xylazine (10 mg/kg) and kept over a heating bed.
Challenges and Improvements of Developing an Ischemia Mouse Model Through Bilateral Common Carotid Artery Occlusion
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2020, Neurobiology of DiseaseCitation Excerpt :Necrotic lesions also involve the caudate putamen, thalamus as well as amygdala (Sonobe et al., 2015). The piriform cortex, cerebellar Purkinje cell layer and hippocampal (CA1-3 and dentate gyrus) neuronal populations were never affected (Fig. 5), in major contrast to the effects of anoxia-induced brain damage in which the deeper layers of cerebral cortex along with hippocampal and neocortical pyramidal cells, striatal neurons, and Purkinje cells (Brierley and Excell, 1966; Graham et al., 1990; Iwasaki et al., 1989) are affected. The lack of memory deficit during MWM testing could be explained by the absence of hippocampal lesions (Sonobe et al., 2015), while the motor deficit and blindness can be accounted for by lesions affecting the thalamus, the motor or visual cortex as well as subcortical nuclei (Fig. 5).