کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8749721 1593673 2018 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Forsythoside A inhibited S. aureus stimulated inflammatory response in primary bovine mammary epithelial cells
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
Forsythoside A inhibited S. aureus stimulated inflammatory response in primary bovine mammary epithelial cells
چکیده انگلیسی
Forsythoside A (FTA), the major bioactive component extracted from Forsythiae fructus, has multiple biological properties especially anti-inflammatory property. Staphylococcus aureus (S. aureus), a Gram-positive organism, is one of most common pathogens that cause bovine mastitis. This study evaluated the anti-inflammatory effect of FTA in S. aureus-stimulated primary bovine mammary epithelial cells (bMEC). Primary bovine mammary epithelial cells were isolated from the mammary tissue of lactating cows and identified as bMEC. The cell viability of bMEC was analyzed by MTT. The bMEC were stimulated with S. aureus in the presence or absence of FTA. Subsequently, the expression level of pro-inflammatory cytokines was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Nuclear factor-κB (NF-κB), inhibitor protein of NF-κB (IκBα), p38, extracellular signal-regulated protein kinase (ERK), and c-JunN-terminal kinase (JNK) were measured by western blotting. The results showed that the cell viability was not affected by the FTA. FTA markedly down-regulated the expressions of TNF-α, IL-1β and IL-6 in S. aureus-stimulated bMEC. In addition, FTA was found to suppress S. aureus-induced NF-κB and MAPKs activation in a dose-dependent manner. These results indicated that FTA exerted anti-inflammatory property in S. aureus-stimulated bMEC by interfering the activation of NF-κB and MAPKs signaling pathways. Thereby, FTA may be a potential therapeutic agent against inflammatory disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 116, March 2018, Pages 158-163
نویسندگان
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