Okadaik Asitle İndüklenen Alzheimer Sıçan Modelinde Betulin Tedavisi ile Çoklu Organ Hasarının COX Aracılığıyla Düzenlenmesi

Abstract

Objective: Alzheimer's Disease (AD) is a progressive neurodegenerative disease. Cyclooxygenases (COXs) are essential in the inflammatory and regenerative processes of AD. This study aims to show that Betulin, a natural phytochemical (triterpene), is a candidate for COX-mediated correction of multiple organ damage of AD. Materials and Methods: In this study, the effects and treatment potential of Betulin were investigated in the kidney, heart, and small intestine tissue in genetic, and histological contexts in an okadaic acid-induced rat AD model. A total of 36 Wistar albino male rats were included in the study. Cyclooxygenase 1 (COX-1) and Cyclooxygenase 2 (COX2) gene expressions were investigated by quantitative real-time PCR (qRT-PCR) in kidney, heart, and small intestine tissues. COX-1 and COX-2 proteins in tissues were analyzed by immunohistochemistry. Results: COX-1 and COX-2 genes were detected to be overexpressed in the AD model. The expression of both genes was increased in the AD model and decreased after betulin treatment. Histological scores showed a strong positive effect of Betulin on the kidney, while it was relatively less effective on the heart and small intestine tissue. Conclusion: In treating organ damage in AD, COXs can be inhibited by Betulin and may be effective in functional recovery.