کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5549051 1556600 2017 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Inhibitory effect of punicalagin on lipopolysaccharide-induced neuroinflammation, oxidative stress and memory impairment via inhibition of nuclear factor-kappaB
ترجمه فارسی عنوان
اثر مهاری پانالالالژین بر التهاب عصبی ناشی از لیپوپلی ساکارید، استرس اکسیداتیو و اختلال حافظه از طریق مهار فاکتور کاپاآب
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب رفتاری
چکیده انگلیسی


- Neuroinflammation and amyloidogenesis are main symptoms of Alzheimer's disease.
- NF-κB activation can induce the inflammation and amyloidogenesis pathways.
- Punicalagin inhibits NF-κB activation through direct binding to its subunit P50.
- Punicalagin reduces LPS-induced neuroinflammation and amyloidogenesis.
- Punicalagin is a possible candidate for treating Alzheimer's disease.

Neuroinflammation is significant in the pathogenesis and development of Alzheimer's disease (AD). Previously, we showed lipopolysaccharide (LPS)-induced neuroinflammation caused memory impairment. We investigated the possible preventive effects of punicalagin (PUN), a component of pomegranate, on memory deficiency caused by LPS, along with the fundamental mechanisms. LPS-treated cultured astrocytes and microglial BV-2 cells were investigated for anti-neuroinflammatory effects of PUN. PUN (1.5 mg/kg) ameliorates LPS (250 μg/kg daily 7 times)-induced memory impairment as well as prevents the LPS-induced expression of inflammatory proteins. In in vitro study, we also found that PUN (1 μg/ml) inhibited the LPS-(10, 20 and 50 μM) induced expression of iNOS and Cox-2 as well as the production of ROS, NO, TNF-α and IL-1β. PUN also suppress activation of NF-κB via inhibition of IκB degradation as well as p50 and p65 translocation into the nucleus in LPS treated mouse brain and cultured astrocytes and microglial BV-2 cells. Consistent with the inhibitory effect on neuro inflammation, PUN inhibited LPS-induced Aβ1-42 generation through down-regulation of APP and BACE1 expression in in vivo and in vitro study. Moreover, PUN directly binds to NF-κB subunit p50 evidenced by a docking model and pull down assay. These results suggest that PUN inhibits LPS-induced memory impairment via anti-inflammatory and anti-amylogenic mechanisms through inhibition of NF-κB activation.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 117, 1 May 2017, Pages 21-32
نویسندگان
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