کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6261592 1613232 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Research reportEffects of naringin on learning and memory dysfunction induced by gp120 in rats
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Research reportEffects of naringin on learning and memory dysfunction induced by gp120 in rats
چکیده انگلیسی


- Naringin may have therapeutic effect on dementia rats induced by gp120.
- Naringin inhibited the up-regulation of P2X7 receptor induced by gp120 in rats.
- Naringin may inhibit BzATP-activated current enhanced by gp120.
- P65 involved in the catabatic effect of naringin on gp120-induced cognitive deficit.

The aim of the present study was to investigate the effects of naringin on learning and memory dysfunction induced by HIV-1-enveloped protein gp120 in rats, and to identify its potential mechanisms of action. Learning and memory ability was evaluated via Morris water maze test, P2X7 receptor and P65 protein expressions in the rat hippocampus were detected by western blot analysis, and P2X7 mRNA expression in the hippocampus was measured by RT-PCR. We also recorded P2X7 agonist BzATP-activated current in the hippocampus via patch clamp technique. The results showed that naringin treatment (30 mg/kg/day) markedly decreased the escape latency and target platform errors of rats treated with gp120 (50 ng/day), and further, that naringin treatment significantly decreased the expression of P2X7 and P65 protein and P2X7 mRNA in the hippocampus of gp120-treated rats. In addition, naringin treatment reduced BzATP-activated current in the hippocampus of gp120-treated rats. These results altogether demonstrated that naringin can improve gp120-induced learning and memory dysfunction via mechanisms involving the inhibition of P2X7 expression in the hippocampus.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 124, June 2016, Pages 164-171
نویسندگان
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