کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4318813 1613253 2014 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Pharmacological benefit of I1-imidazoline receptors activation and nuclear factor kappa-B (NF-κB) modulation in experimental Huntington's disease
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Pharmacological benefit of I1-imidazoline receptors activation and nuclear factor kappa-B (NF-κB) modulation in experimental Huntington's disease
چکیده انگلیسی


• 3-Nitropropionic acid (3-NPA) has induced dementia and Huntington's disease (HD).
• 3-NPA has impaired brain AChE, MDA, SOD, CAT, mitochondrial enzymes.
• Modulation of I1 receptor and NF-κB has attenuated 3-NPA induced dementia & HD.
• I1 receptor and NF-κB modulator have attenuated 3-NPA induced biochemical changes.
• I1 receptor and NF-κB modulator may be explored further for benefits in HD.

Huntington's disease (HD), a neurodegenerative disorder, is characterized by progressive motor dysfunction, emotional disturbances, dementia, weight loss and anxiety.The tremendous amount of research work is required to identify new pharmacological agents of therapeutic utility to combat this condition. This study investigates the effect of selective modulator of I1-imidazoline receptor (moxonidine) as well as nuclear factor kappa-B (NF-κB) (natrium diethyl dithio carbamate trihydrate-NDDCT) on 3-nitropropionic acid (3-NPA) induced experimental HD condition. 3-NPA was used to induce mitochondrial damage and associated HD symptoms in rats. Anxiety was assessed using Elevated plus maze-EPM and learning-memory was assessed using EPM and Morris water maze-MWM. Different biochemical estimations were used to assess brain striatum oxidative stress (lipid peroxide, superoxide dismutase and catalase), nitric oxide levels (nitrite/nitrate), cholinergic activity (brain striatum acetyl cholinesterase activity), and mitochondrial enzyme complex (I, II and IV) activities. 3-NPA has induced anxiety, impaired learning-memory with a reduction in body weight, locomotor activity, grip strength. It has increased brain striatum acetylcholinesterase-AChE activity, oxidative stress (lipid peroxide, nitrite/nitrate, superoxide dismutase and catalase) and impaired mitochondrial complex enzyme (I, II and IV) activities. Tetrabenazine-TBZ (monoamine storage inhibitor) was used as positive control. Treatment with moxonidine, NDDCT and TBZ significantly attenuated 3-NPA induced reduction in body weight, locomotor activity, grip strength, anxiety as well as impaired learning and memory. Administration of these agents attenuated 3-NPA induced various biochemical impairments. Therefore, modulation of I1-imidazoline receptor as well as NF-κB may be considered as potential pharmacological agents for the management of 3-NPA induced HD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 102, March 2014, Pages 57–68
نویسندگان
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