کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6117297 | 1591561 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigallocatechin-3-gallate ameliorates both obesity and autoinflammatory arthritis aggravated by obesity by altering the balance among CD4+ T-cell subsets
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Epigallocatechin-3-gallate (EGCG) is the most biologically active catechin in green tea. EGCG has been shown to have therapeutic effects in autoinflammatory diseases and obesity. Obesity is currently regarded-partly-as an inflammatory condition because of the inflammatory cytokines and higher Th1 cell differentiation detected in obese animal models and human cohort studies. In this work, the effects of EGCG on diet-induced obesity (DIO) mice and obese collagen-induced arthritis (CIA) mice were investigated. EGCG reduced the body weight and fat infiltration in liver tissue while improving serum lipid profiles in DIO mice. EGCG also induced a higher Treg/Th17 cell ratio in CD4+ T-cell differentiation by decreasing the ratio of STAT3/STAT5 expression in DIO mice. EGCG was also effective in obese CIA mice. Reducing Th17 cells and increasing regulatory T (Treg) cells by affecting the STAT protein ratio were important effects of EGCG that might result in improved arthritic scores and levels of several inflammatory indicators. Thus, EGCG has an anti-inflammatory effect by suppressing STAT3 proteins and Th17-cell differentiation. EGCG thus shows promise for treating autoimmune conditions related to STAT3 or Th17 cells, such as metabolic syndrome, inflammatory arthritis, and some neoplastic diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunology Letters - Volume 157, Issues 1â2, JanuaryâFebruary 2014, Pages 51-59
Journal: Immunology Letters - Volume 157, Issues 1â2, JanuaryâFebruary 2014, Pages 51-59
نویسندگان
Jae-Kyeong Byun, Bo-Young Yoon, Joo-Yeon Jhun, Hye-Joa Oh, Eun-kyoung Kim, Jun-Ki Min, Mi-La Cho,