کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4300889 1288426 2013 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ginsenoside Rg1 improves survival in a murine model of polymicrobial sepsis by suppressing the inflammatory response and apoptosis of lymphocytes
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی عمل جراحی
پیش نمایش صفحه اول مقاله
Ginsenoside Rg1 improves survival in a murine model of polymicrobial sepsis by suppressing the inflammatory response and apoptosis of lymphocytes
چکیده انگلیسی

BackgroundUnbalanced inflammatory response and lymphocyte apoptosis are the main reasons for high mortality in patients with sepsis. Ginsenoside Rg1 (Rg1), the most important component isolated from Panax ginseng, has long been used to treat inflammatory and immune-related diseases. We designed this study to investigate the therapeutic effect of this agent on cecal ligation and puncture (CLP)-induced sepsis in mice.Materials and methodsWe randomly divided C57BL/6 mice into four experimental groups: sham, sham plus Rg1, CLP, and CLP plus Rg1. We intravenously injected Rg1 (20 mg/kg) 1 h after CLP and evaluated survival, bacterial clearance, cytokine production, histology, neutrophil emigration, and lymphocyte apoptosis.ResultsOur study showed that treatment with Rg1 significantly improved survival in septic mice (P < 0.01). Rg1 administration suppressed the inflammatory response and enhanced bacterial clearance. Histologic examination of lung and liver showed only minor abnormalities in mice that received Rg1. In addition, Rg1 increased neutrophil counts in peritoneal cavity and inhibited lymphocyte apoptosis in thymus and spleen.ConclusionsGinsenoside Rg1 has a protective role against CLP-induced polymicrobial sepsis by attenuating the proinflammatory response, enhancing innate immunity and preserving adaptive immunity. Rg1 could be a promising new agent for treatment of sepsis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Surgical Research - Volume 183, Issue 2, August 2013, Pages 760–766
نویسندگان
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