دانلود مقاله ISI انگلیسی شماره 72847
عنوان فارسی مقاله

فقدان لذت و پپتید ناتریورتیک قلبی دهلیزی دگرسان بدنبال عوامل استرس زای مزمن و درمان اندوتوکسین در موش

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
72847 2010 8 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
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عنوان انگلیسی
Anhedonia and altered cardiac atrial natriuretic peptide following chronic stressor and endotoxin treatment in mice
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Psychoneuroendocrinology, Volume 35, Issue 2, February 2010, Pages 233–240

کلمات کلیدی
استرس مزمن؛ لیپوپلی ساکارید؛ بافت قلب پولیس ملی؛ پولیس ملی پلاسما، سایتوکاین ها و فقدان لذت؛ افسردگی
پیش نمایش مقاله
پیش نمایش مقاله فقدان لذت و پپتید ناتریورتیک قلبی دهلیزی دگرسان بدنبال عوامل استرس زای مزمن و درمان اندوتوکسین در موش

چکیده انگلیسی

Chronic stressors and inflammatory immune activation may contribute to pathophysiological alterations associated with both major depression and cardiovascular disease. The present study, conducted in mice, assessed whether a chronic stressor of moderate severity that induced an anhedonic effect, when coupled with a bacterial endotoxin, lipopolysaccharide (LPS), additively or interactively provoked circulating and heart atrial natriuretic peptide (ANP), a potentially useful diagnostic and prognostic tool in cardiac diseases. As well, given the potential role of inflammatory processes in both depression and cardiovascular disease, we assessed pro-inflammatory mRNA expression in heart in response to the stressor and the LPS treatments. Male CD-1 mice that had been exposed to a chronic, variable stressor over 4 weeks displayed reduced sucrose consumption, possibly reflecting the anhedonic effects of the stressor. Treatment with LPS (10 μg) provoked increased circulating corticosterone levels in both chronically stressed and non-stressed mice. Moreover, ANP concentrations in plasma and in the left ventricle were increased by both the stressor and the LPS treatments, as were left atrial and ventricular cytokine (interleukin-1β; tumor necrosis factor-α) mRNA expression. Further, these treatments synergistically influenced the rise of plasma ANP. A link may exist between stressor-provoked depressive features (anhedonia) and immune activation, with elevated levels of ANP, a potential marker of cardiovascular disturbance. These findings are consistent with the view that chronic stressors and inflammatory immune activation may represent a common denominator subserving the frequent comorbidity between these illnesses.

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