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  • Title: Evaluation of PECAM-1 and p38 MAPK expressions in cerebellum tissue of rats treated with caffeic acid phenethyl ester: a biochemical and immunohistochemical study.
    Author: Çetin A, Deveci E.
    Journal: Folia Morphol (Warsz); 2019; 78(2):221-229. PubMed ID: 30543083.
    Abstract:
    BACKGROUND: This study aimed to investigate the antioxidative and anti-inflam- matory effects of caffeic acid phenethyl ester (CAPE) on damage caused to cere- bellum tissue by diffuse traumatic head trauma via biochemical, histopathologic, and immuno-histochemical methods. MATERIALS AND METHODS: Male Sprague-Dawley (300-350 g) rats were subjected to traumatic brain injury with a weight-drop device (300 g/1 m weight-height im- pact). Twenty-four adult rats were randomly divided into three equal groups of 8, including a control group, traumatic brain injury (TBI) group, and TBI + CAPE treatment group (10 μmoL/kg/i.p.). Cerebellum tissue samples taken from anterior lobe from all rats were taken 7 days after traumatic injury and were subjected to biochemical and histopathological analysis, as well as immunohistochemical ana- lysis for platelet endothelial cell adhesion molecule-1 (PECAM-1) and phosphate 38-mitogen-activated protein kinase (p38 MAPK). RESULTS: In the TBI group, the granular layer had dilatation and haemorrhage in the capillary vessels and inflammatory cell infiltration around the periphery of the blood vessels. In the TBI + CAPE group, the small capillaries in the white matter were slightly dilated, there were no inflammatory cells, and dense chromatin/ granular cells were observed in the granular layer. Also in the TBI + CAPE group, the Purkinje cells of the ganglion cell layer had ovoid nuclei, were chromatin- -rich, and their extensions protruded to the molecular layer. CAPE is thought to regulate inflammation, cell damage, and angiogenetic development by affecting the PECAM-1 and p38 MAPK proteins. CONCLUSIONS: These proteins are key modulators of endothelial integrity and neuroinflammation in vessels in response to endothelial damage as well as of the proinflammatory response in the cerebellum in response to traumatic damage.
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