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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://repozitorij.uni-lj.si/IzpisGradiva.php?id=185531"><dc:title>Histopathological analysis of the inhibitory effect of ibuprofen on amyloidogenesis in a mouse model</dc:title><dc:creator>Moghaddam,	Atieh Seyedian	(Avtor)
	</dc:creator><dc:creator>Azizzadeh,	Mohammad	(Avtor)
	</dc:creator><dc:creator>Movasseghi,	Ahmad Reza	(Avtor)
	</dc:creator><dc:subject>amyloid A</dc:subject><dc:subject>amyloidosis</dc:subject><dc:subject>casein</dc:subject><dc:subject>ibuprofen</dc:subject><dc:subject>mouse model</dc:subject><dc:description>Amyloidosis represents a group of diseases, all characterized by the deposition of protein fibrils with a β-sheet structure. To evaluate the effects of ibuprofen on the inhibition of amyloid deposition, we used an animal model of experimental amyloid A amyloidosis. BALB/c mice (n = 30) were divided into two groups (n = 15 mice/group). Both the treatment and control groups received casein solution for 3 weeks to induce experimental amyloidosis, and ibuprofen was added to the drinking water of the treatment group simultaneously. After 3 weeks, all mice were euthanized. Tissue samples of various organs were collected, fixed, and processed for routine histopathological examination. This revealed amyloid deposition as an amorphous, homogenous, and eosinophilic substance in the control group’s renal glomeruli, hepatic parenchyma, and splenic vascular walls. In the treatment group, only mild amyloid deposition was observed in renal glomeruli and occasionally in the vascular wall of other tissues. The amount of amyloid deposition in the liver and kidneys in the treatment group was significantly lower than in the control group. Our results suggest that ibuprofen may prevent amyloid formation and accumulation in mice, especially in the kidneys and liver.</dc:description><dc:date>2025</dc:date><dc:date>2026-08-07 12:44:39</dc:date><dc:type>Članek v reviji</dc:type><dc:identifier>185531</dc:identifier><dc:language>sl</dc:language></rdf:Description></rdf:RDF>
