茯砖茶提取物对葡聚糖硫酸钠诱导小鼠炎症性肠病的保护作用研究

doi:10.13305/j.cnki.jts.2019.06.003

摘要/Abstract

摘要： 茯砖茶是我国特有的一种黑茶。本文以茯砖茶为原料,分别制备了茯砖茶水提物（FWE）、经95%乙醇沉后得到的醇溶物（FES）和醇沉物（FEP）,并探究了3种提取物对葡聚糖硫酸钠诱导小鼠炎症性肠病的保护作用。研究表明,3种茯砖茶提取物都能够减轻炎症性肠病的肠道结构损伤,其中FWE组效果最好;同时茯砖茶提取物可以显著提升小鼠血清和肠道组织上清液中超氧化物岐化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽（GSH）水平以及降低白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）水平,且作用效果均为FWE组>FES组>FEP组;在蛋白水平上,FWE组小鼠肠道组织的NF-κB p65蛋白水平有所降低;IκBα的蛋白水平在FWE组和FES组中有所增加;核因子E2相关因子2（Nrf2）和血红素氧化酶-1（HO-1）的相关蛋白水平在FWE组和FES组也有所增加。综上所述,茯砖茶提取物可以通过抗氧化和抗炎途径对葡聚糖硫酸钠诱导小鼠炎症性肠病发挥预防保护作用。

关键词: 茯砖茶, 炎症性肠病（IBD）, 炎症, 氧化应激

Abstract: Fu brick tea is a special dark tea in China. In the present work, three extracts, including Fu brick tea water extract (FWE), Fu brick tea ethanol soluble fraction (FES) and Fu brick tea ethanol precipitation fraction(FEP), were prepared and used to further explore their protective effects on inflammatory bowel disease in mice. Researches show that all the Fu brick tea extracts could alleviate the intestinal structure damage of IBD mice. Moreover, the extracts increased the activities of SOD, CAT and the levels of GSH and reduced the levels of IL-6, IL-1β, TNF-α in serum and colon tissue supernatant of mice. Furthermore, the protein level of NF-κB p65 in the colon tissues in the FWE group was decreased compared to the model group. The protein level of IκBα was increased in the FWE group and FES group. Levels of Nrf2 and HO-1 were also increased in the FWE and FES groups. In conclusion, Fu brick tea extracts had a protective effect on IBD mice induced by DSS.

Key words: Fu brick tea, inflammatory bowel disease, inflammation, oxidative stress

中图分类号:

S571.1
R574

胡安恺, 姚立筠, 赵悦伶, 刘畅, 王岳飞, 徐平. 茯砖茶提取物对葡聚糖硫酸钠诱导小鼠炎症性肠病的保护作用研究[J]. 茶叶科学, 2019, 39(6): 641-651. doi: 10.13305/j.cnki.jts.2019.06.003.

HU Ankai, YAO Liyun, ZHAO Yueling, LIU Chang, WANG Yuefei, XU Ping. Protective Effects of Fu Brick Tea Extracts on Inflammatory Bowel Disease Induced by Dextran Sulfate Sodium in Mice[J]. Journal of Tea Science, 2019, 39(6): 641-651. doi: 10.13305/j.cnki.jts.2019.06.003.

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