Animal sciences & veterinary medicines |
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Protective effect and mechanism of matcha on liver lipid accumulation and inflammatory response induced by high-fat diet in mice |
Jihong ZHOU1(),Yue'er YU1,Lejia DING1,Ping XU1,Limin MAO1,2,Yuefei WANG1() |
1.Tea Research Institute, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou 310058, China 2.Zhejiang Tea Group Co. , Ltd. , Hangzhou 310058, China |
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Abstract In this study, we analyzed the main chemical components of matcha made from four tea cultivars, established a high-fat diet-induced C57BL/6J obese mouse model, and selected ‘Maolü’ matcha as an experimental dietary supplement with three doses of 0.1%, 0.5% and 1.0%. The results showed that matcha could reduce body mass gain, blood glucose level rise and liver lipid accumulation induced by the high-fat diet without affecting food intake, and the effect was concentration-dependent. Furthermore, we detected the liver function, oxidative stress level and inflammatory response in mice, and the results showed that dietary supplementation of 1.0% matcha significantly inhibited the abnormal increase of activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) induced by a high-fat diet in liver, and increased the activity of antioxidant enzyme. The expression levels of inflammatory factors, Toll-like receptor 4 (TLR4) and MyD88 were also significantly reduced. In conclusion, matcha effectively improves obesity-related fatty liver lesions and inflammation, and its potential mechanism is to inhibit the activation of the TLR4/MyD88 signaling pathway.
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Received: 11 July 2021
Published: 03 September 2022
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Corresponding Authors:
Yuefei WANG
E-mail: zhoujihong@zju.edu.cn;zdcy@zju.edu.cn
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抹茶对高脂饮食诱导的小鼠肝脏脂质积累和炎症反应的保护作用及机制
本研究比较分析了4个茶树品种抹茶主要化学成分含量的差异,并选取‘茂绿’品种抹茶对高脂饮食诱导的C57BL/6J肥胖小鼠模型进行0.1%、0.5%、1.0% 3种剂量的膳食补充。结果表明,抹茶能够在不影响摄食量的情况下改善高脂饮食导致的体质量增长、血糖水平升高和肝脏脂质积累,且效果呈现出浓度依赖性。进一步对小鼠肝脏功能、氧化应激水平和炎症反应情况进行检测,发现膳食添加1.0%的抹茶能够显著抑制高脂饮食诱导的肝脏谷丙转氨酶(alanine aminotransferase, ALT)和谷草转氨酶(aspartate aminotransferase, AST)活性异常升高,提升抗氧化酶活性,降低炎症因子表达水平,并下调Toll样受体4(Toll-like receptor 4, TLR4)和下游MyD88基因的表达。综上所述,抹茶能够有效改善食源性肥胖和高脂饮食诱发的肝脏脂肪性病变与炎症反应,对TLR4/MyD88信号通路的抑制是其潜在的作用机制。
关键词:
抹茶,
肥胖,
非酒精性脂肪性肝病,
氧化应激,
炎症因子
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|
[1] |
MONGRAW-CHAFFIN M, FOSTER M C, ANDERSON C A M, et al. Metabolically healthy obesity, transition to metabolic syndrome, and cardiovascular risk[J]. Journal of the American College of Cardiology, 2018, 71(17): 1857-1865. DOI:10.1016/j.jacc.2018.02.055
doi: 10.1016/j.jacc.2018.02.055
|
|
|
[2] |
ESLAM M, VALENTI L, ROMEO S. Genetics and epigenetics of NAFLD and NASH: clinical impact[J]. Journal of Hepatology, 2018, 68(2): 268-279. DOI:10.1016/j.jhep.2017.09.003
doi: 10.1016/j.jhep.2017.09.003
|
|
|
[3] |
HUANG J B, LI W J, LIAO W J, et al. Green tea polyphenol epigallocatechin-3-gallate alleviates nonalcoholic fatty liver disease and ameliorates intestinal immunity in mice fed a high-fat diet[J]. Food & Function, 2020, 11(11): 9924-9935. DOI:10.1039/d0fo02152k
doi: 10.1039/d0fo02152k
|
|
|
[4] |
ROCHA A, BOLIN A P, CARDOSO C A L, et al. Green tea extract activates AMPK and ameliorates white adipose tissue metabolic dysfunction induced by obesity[J]. European Journal of Nutrition, 2016, 55(7): 2231-2244. DOI:10.1007/s00394-015-1033-8
doi: 10.1007/s00394-015-1033-8
|
|
|
[5] |
刘东娜,聂坤伦,杜晓,等.抹茶品质的感官审评与成分分析[J].食品科学,2014,35(2):168-172. DOI:10.7506/spkx1002-6630-201402031 LIU D N, NIE K L, DU X, et al. Sensory evaluation and chemical composition of matcha[J]. Food Science, 2014, 35(2): 168-172. (in Chinese with English abstract)
doi: 10.7506/spkx1002-6630-201402031
|
|
|
[6] |
ZHOU J H, LIN H Y, XU P, et al. Matcha green tea prevents obesity-induced hypothalamic inflammation via suppressing the JAK2/STAT3 signaling pathway[J]. Food & Function, 2020, 11(10): 8987-8995. DOI:10.1039/d0fo01500h
doi: 10.1039/d0fo01500h
|
|
|
[7] |
YING L, KONG D D, GAO Y Y, et al. In vitro antioxidant activity of phenolic-enriched extracts from Zhangping Narcissus tea cake and their inhibition on growth and metastatic capacity of 4T1 murine breast cancer cells[J]. Journal of Zhejiang University—Science B, 2018, 19(3): 199-210. DOI:10.1631/jzus.B1700162
doi: 10.1631/jzus.B1700162
|
|
|
[8] |
全国茶叶标准化技术委员会. 抹茶: [S].北京:中国标准出版社,2017. DOI:10.16993/bak National Technical Committee 339 on Tea of Standardization Administration of China.Matcha: GB/T 34778—2017[S]. Beijing: Standards Press of China, 2017. (in Chinese)
doi: 10.16993/bak
|
|
|
[9] |
LI Y, RAHMAN S U, HUANG Y Y, et al. Green tea polyphenols decrease weight gain, ameliorate alteration of gut microbiota, and mitigate intestinal inflammation in canines with high-fat-diet-induced obesity[J]. The Journal of Nutritional Biochemistry, 2020, 78: 108324. DOI:10.1016/j.jnutbio.2019.108324
doi: 10.1016/j.jnutbio.2019.108324
|
|
|
[10] |
LU J, FANG B C, HUANG Y X, et al. Epigallocatechin-3-gallate protects against 1, 3-dichloro-2-propanol-induced lipid accumulation in C57BL/6J mice[J]. Life Sciences, 2018, 209: 324-331. DOI:10.1016/j.lfs.2018.08.007
doi: 10.1016/j.lfs.2018.08.007
|
|
|
[11] |
SELLAYAH D, CAGAMPANG F R, COX R D. On the evolutionary origins of obesity: a new hypothesis[J]. Endocrinology, 2014, 155(5): 1573-1588. DOI:10.1210/en.2013-2103
doi: 10.1210/en.2013-2103
|
|
|
[12] |
YOUNOSSI Z M, KOENIG A B, ABDELATIF D, et al. Global epidemiology of nonalcoholic fatty liver disease-meta-analytic assessment of prevalence, incidence, and outcomes[J]. Hepatology, 2016, 64(1): 73-84. DOI:10.1002/hep.28431
doi: 10.1002/hep.28431
|
|
|
[13] |
WREE A, BRODERICK L, CANBAY A, et al. From NAFLD to NASH to cirrhosis: new insights into disease mechanisms[J]. Nature Reviews Gastroenterology & Hepatology, 2013, 10(11): 627-636. DOI:10.1038/nrgastro.2013.149
doi: 10.1038/nrgastro.2013.149
|
|
|
[14] |
KOLÁČKOVÁ T, KOLOFIKOVA K, SYTAŘOVÁ I, et al. Matcha tea: analysis of nutritional composition, phenolics and antioxidant activity[J]. Plant Foods for Human Nutrition, 2020, 75(1): 48-53. DOI:10.1007/s11130-019-00777-z
doi: 10.1007/s11130-019-00777-z
|
|
|
[15] |
KANG H H, KIM I K, LEE H I, et al. Chronic intermittent hypoxia induces liver fibrosis in mice with diet-induced obesity via TLR4/MyD88/MAPK/NF-κB signaling pathways[J]. Biochemical and Biophysical Research Communications, 2017, 490: 349-355. DOI:10.1016/j.bbrc.2017.06.047
doi: 10.1016/j.bbrc.2017.06.047
|
|
|
[16] |
HOTAMISLIGIL G S. Inflammation, metaflammation and immunometabolic disorders[J]. Nature, 2017, 542(7640): 177-185. DOI:10.1038/nature21363
doi: 10.1038/nature21363
|
|
|
[17] |
CANI P D, AMAR J, IGLESIAS M A, et al. Metabolic endotoxemia initiates obesity and insulin resistance[J]. Diabetes, 2007, 56(7): 1761-1772. DOI:10.2337/db06-1491
doi: 10.2337/db06-1491
|
|
|
[18] |
DE ASSUNCÃO S N F, SORTE N C A B, DE ARAGÃO DANTAS ALVES C, et al. Inflammatory cytokines and non-alcoholic fatty liver disease (NAFLD) in obese children and adolescents[J]. Nutricion Hospitalaria, 2018, 35: 78-83. DOI:10.20960/nh.1317
doi: 10.20960/nh.1317
|
|
|
[19] |
HENAO-MEJIA J, ELINAV E, JIN C C, et al. Inflammasome-mediated dysbiosis regulates progression of NAFLD and obesity[J]. Nature, 2012, 482(7384): 179-185. DOI:10.1038/nature10809
doi: 10.1038/nature10809
|
|
|
[20] |
NAGPAL K, PLANTINGA T S, WONG J, et al. A TIR domain variant of MyD88 adapter-like (Mal)/TIRAP results in loss of MyD88 binding and reduced TLR2/TLR4 signaling[J]. Journal of Biological Chemistry, 2009, 284(38): 25742-25748. DOI:10.1074/jbc.M109.014886
doi: 10.1074/jbc.M109.014886
|
|
|
[21] |
MILANSKI M, DEGASPERI G, COOPE A, et al. Saturated fatty acids produce an inflammatory response predominantly through the activation of TLR4 signaling in hypothalamus: implications for the pathogenesis of obesity[J]. Journal of Neuroscience, 2009, 29(2): 359-370. DOI:10.1523/Jneurosci.2760-08.2009
doi: 10.1523/Jneurosci.2760-08.2009
|
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