随着对棕色脂肪组织（BAT）在成人体内具有生物学功能的肯定，棕色脂肪已经成为当今医学研究的热点。采用动物实验、病理组织学方法及免疫组化，观察了表没食子儿茶素没食子酸酯（EGCG）对棕色脂肪代谢的影响。结果表明，在体重和鼠龄相近时，不同种属小鼠肩甲间棕色脂肪组织HE 染色后的形态不同，C57BL/6 脂肪细胞中的空泡大，胞浆含量少，BALB/c 小鼠脂肪细胞中的空泡小，胞浆含量多，昆明小鼠居中。给昆明小鼠口服不同剂量EGCG 后，150 mg/kg EGCG 能降低小鼠体重的增长，降低附睾周围白色脂肪组织的重量，但没有统计学意义。同时，EGCG 能降低棕色脂肪细胞内脂肪含量，增加胞浆含量，具有统计学意义（P<0.001）。免疫组化结果表明，EGCG 能增加棕色脂肪细胞内脱偶联蛋白1（UCP1）的表达，增加能量代谢。因此，不同种属小鼠的BAT 具有不同的组织形态学特点，这为研究BAT 小鼠的选择提供了依据；EGCG 能够调节小鼠棕色脂肪的代谢功能，这为进一步研究作用机制打下了基础，同时为茶叶在脂肪代谢方面的调节提供了一种新的思路和依据。
With recognition of biological functions of brown adipose tissue (BAT) in adults, it has become a hot topic in medical research. In the present study, the effects of (-)-Epigallocatechin-3-gallate(EGCG) on the metabolism of BAT are investigated through animal experiments, histopathologicaland immunohistochemical methods. The results show that there are disparities in morphology of interscapular BAT among different species of mice. Vacuoles of fat droplets in adipocytes of C57BL/6 mice are the largest, and the cytoplasmic content is the least. Vacuoles in adipocytes of BALB/c mice are the smallest, and the cytoplasmic content is the most. Vacuoles and cytoplasmic content in Kunming mice lie between those in C57BL/6 and BALB/c mice. EGCG at 150 mg/kg decreases the increment rate of body weight and reduces the weights of epididymal white adipose tissue, but there is no statistical significance after different doses of EGCG are administered p.o. to Kunming mice. EGCG significantly decreases the content of fat (shown as vacuoles in the sections) in BAT and increases the cytoplasmic content (P<0.001). By immunohistochemical examination, EGCG increases the expression level of uncoupling protein 1, indicating the increase of energymetabolism in BAT. Therefore, there exist diversemorphological characteristics in different inbred lines of mice, which provides the basis for selection of mice in BAT studies. EGCG may regulate the metabolism of BAT in mice, which lays the foundation for further studies of its mechanism and provides new ideas for studies of the regulation of fat metabolism by tea.
[1] 陈淑珍, 甄永苏. 茶多酚的分子作用靶点及其在抗肿瘤药物实验治疗中的作用[J]. 药学学报, 2013, 48(1): 1-7. Chen Shuzhen, Zhen Yongsu. Molecular targets of tea polyphenols and its roles of anticancer drugs in experimental therapy[J]. Acta Pharmaceutica Sinica, 2013, 48(1): 1-7.
[2] 罗居东, 薛姣, 葛欣, 等. PPARα活化增加肿瘤细胞对EGCG的敏感性的机制[J]. 科技导报, 2013, 31(27): 21-26. Luo Judong, Xue Jiao, Ge Xin, et al. Mechanism of sensitizing effect of PPARα activation on epigallocatechin-3-gallate (EGCG) in cancer cells[J]. Science & Technology Reviews, 2013, 31(27): 21-26.
[3] Kim J, Kim H S, Quon M J. New insights into the mechanisms of polyphenols beyond antioxidant properties; lessons from the green tea polyphenol, epigallocatechin 3-gallate[J]. Redox Biology, 2014, 2: 187-195.
[4] Chan C Y, Wei L, Castro-Muozledo F, et al. (-)-Epigallocatechin-3-gallate blocks 3T3-L1 adipose conversion by inhibition of cell proliferation and suppression of adipose phenotype expression[J]. Life Sciences, 2011, 89(21): 779-785.
[5] Rosenwald M, Wolfrum C. The origin and definition of brite versus white and classical brown adipocytes[J]. Adipocyte, 2014, 3(1): 4-9.
[6] Seale P, Bjork B, Yang W, Kajimura S, et al. PRDM16 controls a brown fat/skeletal muscle switch[J]. Nature, 2008, 454(7207): 961-967.
[7] Truong M T, Erasmus J J, Munden R F, et al. Focal FDG uptake in mediastinal brown fat mimicking malignancy: A potential pitfall resolved on PET/CT[J]. American Journal of Roentgenology, 2004, 183(4): 1127- 1132.
[8] Silva F J, Holt D J, Vargas V, et al. Metabolically active human brown adipose tissue derived stem cells[J]. Stem Cells, 2014, 32(2): 572-581.
[9] Gilsanz V, Hu H H, Kajimura S. Relevance of brown adipose tissue in infancy and adolescence[J]. Pediatric Research, 2012, 73(1): 3-9.
[10] 黄海艳, 钱淑文, 汤其群. 诱导性产热脂肪的性质、诱导因素及潜在临床应用[J]. 中国细胞生物学学报, 2013, 35(9): 1259-1271. Huang Haiyan, Qian Shuwen, Tang Qiqun. Characterization of the inducible thermogenic adipose tissue and its potential application in treatment of obesity and related complications[J]. Chinese Journal of Cell Biology, 2013, 35(9): 1259-1271.
[11] Prats C, Gomez-Cabello A, Nordby P, et al. An optimized histochemical method to assess skeletal muscle glycogen and lipid stores reveals two metabolically distinct populations of type I muscle fibers[J]. Plos One, 2013, 8(10): e77774.
[12] Zhou J, Farah B L, Sinha RA, et al. Epigallocatechin- 3- gallate (EGCG), a green tea polyphenol, stimulates hepatic autophagy and lipid clearance[J]. PLoS One, 2014, 9(1): e87161.
[13] Byun J K, Yoon B Y, Jhun J Y, et al. Epigallocatechin-3-gallate ameliorates both obesity and autoinflammatory arthritis aggravated by obesity by altering the balance among CD4+ T-cell subsets[J]. Immunology Letters, 2014, 157(1): 51-59.
[14] Ohno H, Shinoda K, Ohyama K, et al. EHMT1 controls brown adipose cell fate and thermogenesis through the PRDM16 complex[J]. Nature, 2013, 504(7478): 163-167.
[15] Kajimura S, Seale P, Kubota K, et al. Initiation of myoblast to brown fat switch by a PRDM16-C/EBP-β transcriptional complex[J]. Nature, 2009, 460(7259): 1154-1158.
[16] Okamatsu-Ogura Y, Fukano K, Tsubota A, et al. Thermogenic ability of uncoupling protein 1 in beige adipocytes in mice[J]. Plos One, 2013, 8(12): e84229.
[17] Stier A, Bize P, Habold C, et al. Mitochondrial uncoupling prevents cold- induced oxidative stress: A case study using UCP1 knockout mice[J]. The Journal of Experimental Medicine, 2014, 217(4): 624- 630.
