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DOI 10.1016/j.imlet.2013.11.006

Медицинская библиотека · Immunology letters · 2013

Epigallocatechin-3-gallate ameliorates both obesity and autoinflammatory arthritis aggravated by obesity by altering the balance among CD4+ T-cell subsets.

Byun Jae-Kyeong, Yoon Bo-Young, Jhun Joo-Yeon, Oh Hye-Joa, Kim Eun-kyoung, Min Jun-Ki, Cho Mi-La

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

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.

Для цитирования: Byun Jae-Kyeong, Yoon Bo-Young, Jhun Joo-Yeon, Oh Hye-Joa, Kim Eun-kyoung, Min Jun-Ki, Cho Mi-La. Epigallocatechin-3-gallate ameliorates both obesity and autoinflammatory arthritis aggravated by obesity by altering the balance among CD4+ T-cell subsets.. Immunology letters. 2013. DOI: 10.1016/j.imlet.2013.11.006.

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