綠茶表沒食子兒茶素沒食子酸酯藉由微核醣核酸-143/蛋白δ同源物1路徑抑制3T3-L1前脂肪細胞的生長;Green tea epigallocatechin gallate inhibits 3T3-L1 preadipocyte growth through the microRNA-143/DLK1 pathways

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題名:	綠茶表沒食子兒茶素沒食子酸酯藉由微核醣核酸-143/蛋白δ同源物1路徑抑制3T3-L1前脂肪細胞的生長;Green tea epigallocatechin gallate inhibits 3T3-L1 preadipocyte growth through the microRNA-143/DLK1 pathways
作者:	陳嘉珮;Chen, Chia-Pei
貢獻者:	生命科學系
關鍵詞:	脂肪;小分子核糖核酸;表沒食子兒茶素沒食子酸酯;Adipocyte;MicroRNA;EGCG
日期:	2020-07-08
上傳時間:	2020-09-02 15:26:17 (UTC+8)
出版者:	國立中央大學
摘要:	據以前報導指出，綠茶兒茶素（GTCs）和小分子核糖核酸（miR）可分別通過改變脂肪細胞的有絲分裂和成脂過程來調節肥胖的發展。但是尚未發現有關綠茶的miR介導效應，特別是表沒食子兒茶素沒食子酸酯（EGCG）對脂肪細胞生長的影響的研究。使用3T3-L1白色前脂肪細胞，我們發現EGCG上調了20個miR分子（例如，mmu-miR-1224-5p，mmu-miR-711和mmu-miR-8108），而下調了20個miR分子（例如mmu-miR -668-3p和mmu-miR-690）。進一步RT-qPCR分析證實，EGCG時間和劑量依賴性地誘導3T3-L1前脂肪細胞miR-143和miR-let-7a水平的增加。且EGCG對miR-155的表達沒有影響，但顯著降低了Pref-1 / DLK1（miR-143的靶標）和HMGA2（miR-let-7a的靶標）mRNA和蛋白質的表現。這些數據顯示EGCG對特定類型miR家族成員具有選擇性作用。此外，在缺少EGCG的情況下，過度表達miR-143或miR-let-7a通過細胞數量的減少和降低細胞活力抑制了3T3-L1前脂肪細胞的生長。而處理miR-143抑制劑可拮抗EGCG對細胞數量和細胞活力的抑制作用。這些數據顯示，EGCG對前脂肪細胞生長具有miR-143依賴性。有趣的是，EGCG類似物穀胱甘肽激活劑，如N-乙醯半胱氨酸，刺激miR-143和miR-let-7a的表現量，而使用穀胱甘肽抑製劑（如丁硫氨酸亞碸亞胺）預處理可阻斷EGCG的作用。此外，發現AMPK抑製劑，如化合物C，可以逆轉EGCG對miR-143和miR-let-7基因表達的影響。總之，EGCG可能通過穀胱甘肽和AMPK的方式激活miR-143和miR-let-7a分子來抑制前脂肪細胞的生長。;Green tea catechins (GTCs) and microRNA (miR) molecules have been reported to regulate development of obesity, respectively, as characterized by changes in the mitogenic and adipogenic processes of fat cells. No studies were found on the miR-mediated effects of GTC, particularly epigallocatechin gallate (EGCG), on fat cell growth. Using 3T3-L1 white preadipocytes, we found that EGCG upregulated 20 miR molecules (e.g., mmu-miR-1224-5p, mmu-miR-711, and mmu-miR-8108) and downregulated 20 miR molecules (e.g., mmu-miR-668-3p and mmu-miR-690). Further RT-qPCR analysis confirmed that EGCG time- and dose-dependently induced increases in miR-143 and miR-let-7a levels in 3T3-L1 preadipocytes. EGCG had no effect on miR-155 expression, but it significantly induced decreases in levels of Pref1/DLK1 (a target of miR-143) and HMGA2 (a target of miR-let-7a) mRNAs and proteins. These data suggest the selective effect of EGCG on particular types of miR family members. In addition, over-expression of either miR-143 or miR-let-7a inhibited 3T3-L1 preadipocyte growth in the absence of EGCG, as indicated by decreased cell number and by reduced cell viability. Whereas, treatment with the inhibitor of miR-143 antagonized the inhibitory effect of EGCG on cell number and cell viability. These data suggest a miR-143-dependent effect of EGCG on preadipocyte growth. Interestingly, EGCG mimicked the glutathione activator, such as N-acetyl-cysteine, to stimulate miR-143 and miR-let-7a, and pretreatment with the glutathione inhibitor, such as buthionine sulphoximine, blocked such EGCG effects. Moreover, an AMPK inhibitor, such as compound C, was found to reverse the effects of EGCG on miR-143 and miR-let-7 gene expressions. In conclusions, EGCG inhibits the growth of preadipocytes through activations of miR-143 and miR-let-7a molecules in glutathione- and AMPK-dependent ways.
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