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JCR 2016
جستجوی مقالات
جمعه 25 مهر 1404
Physiology and Pharmacology
، جلد ۲۹، شماره ۳، صفحات ۲۶۰-۲۷۱
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
The role of Bufexamac in reducing anxiety levels: focus on HPA axis dysfunction and neurotransmitter regulation in a rat model of Alzheimer’s disease
چکیده انگلیسی مقاله
Introduction:
Alzheimer’s disease (AD) is a neurocognitive disorder characterized by neuropsychiatric symptoms (NPS), particularly anxiety. The underlying mechanisms involve disruptions in the hypothalamic-pituitary-adrenal (HPA) axis, and altered serotonergic signaling due to amyloid-beta (Aβ) accumu-lation. This study investigates the effects of Bufexamac, a Cyclooxygenase-2 (COX-2), and HDAC Class IIb inhibitor, on anxiety-like behaviors and neurochemical changes in a rat model of AD induced by Aβ.
Methods:
18 adult Wistar rats were divided into three groups: Saline, Aβ, and Aβ + Bufexamac. Aβ25-35 was administered via intracerebroventricular injection, followed by daily Bufexamac treatment for eight days. Anxiety-like behaviors were assessed using the open-field test, while Western blotting and ELISA measured levels of glucocorticoid receptors (GR), corticotropin releasing factor (CRF), and serotonin in the amygdala.
Results:
Bufexamac significantly mitigated Aβ-induced anxiety-like behaviors, as evidenced by increased line crossings and time spent in the center of the arena (P<0.05). Western blot analysis revealed that Bufexamac reduced elevated GR levels in the Aβ group (P<0.05). Additionally, Bufexamac treat-ment significantly regulated serotonin (P<0.01) and CRF levels (P<0.05) in the amygdala compared to the Aβ group.
Conclusion:
Bufexamac effectively alleviates anxiety-like behaviors and restores neurochemical alterations in a rat model of AD, suggesting its potential as a possible therapeutic agent targeting neuropsychiatric symptoms associated with AD. Further research is warranted to explore its clinical applicability.
کلیدواژههای انگلیسی مقاله
Alzheimer’s disease,Bufexamac,Glucocorticoid receptor,Serotonin,Histone deacetylase inhibitors
نویسندگان مقاله
| Monireh Mirehei
Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| Fereshteh Motamedi
Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| Nader Maghsoudi
Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| Fariba Khodagholi
Neuroscience Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| Fatemeh Abbaszadeh
Neurobiology Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran
نشانی اینترنتی
http://ppj.phypha.ir/browse.php?a_code=A-10-1618-2&slc_lang=en&sid=1
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کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
Neurophysiology/Pharmacology
نوع مقاله منتشر شده
Experimental research article
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