چکیده مقاله :
بیماری آلزایمر یک اختلال تخریبی نورونی است که باعث مرگ نورون و از دست دادن حافظه می شود و موجب تولید رادیکال های آزاد و فاکتورهای التهابی بروز می کند. مطالعات نشان می دهد بورنیل استات به عنوان یک مونوترپن دارای اثرات آنتی اکسیدانی و ضد التهابی می باشد. بنابراین در این مطالعه اثرات بورنیل استات با دوزهای20 و 50 میلی گرم/کیلوگرم در موش آلزایمری شده نر نژاد ویستار مورد بررسی قرار گرفت . برای ایجاد مدل آلزایمری از تزریق دو طرفه Aβ1-42 درون هیپوکامپ رتهای نر استفاده شد. در این مطالعه آنزیم های بیوشیمیایی SOD و MDA، تست رفتاری شاتل باکس، بررسی های هیستولوژیکی و رنگ آمیزی هماتوکسیلین و ائوزین و تیوفیلاوین S جهت بررسی نوروژنز و پلاک های آمیلوئیدی و اثرات استرس بی حرکتی کوتاه مدت بر موشهای آلزایمری و همچنین اثرات ترکیب ذکر شده در محیط in vitro نیز مورد بررسی قرار گرفت. فاکتورهای بیوشیمیایی، تصاویر بافت شناسی و آزمون رفتاری گروه آلزایمری در مقایسه با گروه های کنترل به طور معناداری متفاوت بود . به طوریکه شاخص های یادگیری و حافظه در گروه آلزایمری شده در مقایسه با گروه کنترل کاهش معنا داری نشان داد. همچنین دریافت ترکیب بورنیل استات باعث افزایش معنادار نوروژنز و کاهش معنادار تراکم پلاک ها و همچنین تغییرات شاخص های بیوشیمیایی و آزمون رفتاری شد. علاوه بر این، دریافت ترکیب بورنیل استات توام با استرس بی حرکتی باعث افزایش سرعت یاد گیری و بهبود حافظه نسبت به گروه آلزایمری شد. قابل ذکر است که ترکیب فوق در محیط in vitro باعث کاهش فیبریل های آمیلوئیدی شد. با توجه به نتایج به دست آمده در این مطالعه و گزارشهای قبلی مبنی بر اثرات ضد التهابی و آنتی اکسیدان بورنیل استات به نظر میرسد این ترکیب میتوانند اختلالات و عارضههای ایجاد شده در حافظه را بهبود ببخشند.
چکیده انگلیسی:
Alzheimer's disease is a neurodegenerative disorder that results in neuronal death and memory loss as it progresses. Following the progression of this disease, the production of free radicals and inflammatory factors occurs and it is now increasingly widespread, especially among the elderly. Studies show that Bornyl acetate, as a monoterpene, has antioxidant and anti-inflammatory effects. Therefore, the present study aims at assessing the effects of Bornyl acetate on AD male Wistar rats. Aβ1-42 was injected into the hippocampus of male rats bilaterally to create the Alzheimer's model. The therapeutic as well as the preventive effects of Bornyl acetate at a dosage (50, 20 mg/kg) were also investigated. Moreover, biochemical enzymes, SOD and MDA, shuttle box behavioral test, histological studies and hematoxylin & eosin and thioflavin-S staining were used to evaluate neurogenesis and amyloid plaques and the effects of short-term restraint stress on AD rats as well as the effects of the compound in vitro. Biochemical factors, histological images and behavioral test of the AD group were significantly different from the control groups and AD group showed a significant decline in learning and memory indices compared with the control group. Also, receiving a Bornyl acetate caused a significant increase in neurogenesis and a significant decrease in plaque density as well as significant changes in biochemical indices and behavioral tests. In addition, Bornyl acetate + restraint stress (R) group elevated learning speed and improved memory compared with the AD group. Notably, the above combination reduced amyloid fibrils in vitro. It seems that this compound can improve memory disorders and complications according to the results of the present study and previous reports suggest the anti-inflammatory and antioxidant effects of Bornyl acetate.
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