Cerebral inhibition of the H۳K۹ methylation could ameliorate blood-brain barrier dysfunction and neural damage in vascular dementia
- سال انتشار: 1403
- محل انتشار: مجله آرشیو رازی، دوره: 79، شماره: 5
- کد COI اختصاصی: JR_ARCHRAZI-79-5_014
- زبان مقاله: انگلیسی
- تعداد مشاهده: 140
نویسندگان
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
۱Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran ۲Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
چکیده
Dementia is a broad category of brain diseases denoting various brain diseases with degenerative or vascular components that cause a long-term and often gradual decrease in the ability to think and remember severe enough to affect daily functioning. Literature has indicated that the G۹a/GLP enzyme, through upregulating histone ۳ lysine ۹ dimethylation (H۳K۹me۲), is a major effector in VD. In such a way that the increase of H۳K۹ methylation by G۹a/GLP during vascular dementia leads to inhibiting the expression of neuroprotective proteins and also reduces the expression of proteins that play a crucial role in the blood brain barrier function.Using a model of permanent common carotid arteries (CCA) occlusion, we investigated the impact of a G۹a/GLP inhibitor (BIX۰۱۲۹۴) on VD. After occlusion of the CCA, BIX۰۱۲۹۴ (۲۲.۵µg.kg-۱ ) was given intraperitoneally three times a week for a month. Nissl staining, Evans blue, and brain water content were assessed and western blot analysis was used to evaluate the hippocampal levels of Bax and Bcl۲.Using BIX۰۱۲۹۴ enhanced blood-brain barrier stability (P < ۰.۰۵) and subsequently reduced brain edema in comparison to the VD group (P < ۰.۰۵ for both). Neural injury in the CA۱ area of the treatment group decreased by BIX۰۱۲۹۴ injection when compared to the VD group (P< ۰.۰۵). On the other hand, the Bax/Bcl۲ ratio considerably decreased in the treatment group (P < ۰.۰۰۰۱). To summarize, our research shows that inhibiting H۳K۹ methylation can prevent the development of vascular dementia by reducing the level of cerebral edema and neural apoptosis in the hippocampus area after ischemic stroke.کلیدواژه ها
H۳K۹, Brain edema, Blood-brain barrier, Vascular dementia, Cerebral ischemiaاطلاعات بیشتر در مورد COI
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