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Journal of Tea Science ›› 2020, Vol. 40 ›› Issue (2): 165-172.doi: 10.13305/j.cnki.jts.2020.02.003

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Effects of ‘Eurotium cristatum Loose Tea’ and ‘Eurotium cristatum Powder’ on the Expressions of JAK2/STAT3 Inflammation and Phosphorylated Proteins in Lung Tissue of Passive Smoking Mice

ZENG Hongzhe1, HUANG Xiangxiang1, YU Lijun1,2,3*, ZHOU Yufei1, XU Shuai1, QU Furong1   

  1. 1. Tea Science Department, College of Horticulture, Hunan Agricultural University, Changsha 410128, China;
    2. Key Lab of Tea Science of Ministry of Education, Hunan Agricultural University, Changsha 410128, China;
    3. National Research Center of Engineering Technology for Utilization of Botanical Functional Ingredients, Changsha 410128, China
  • Received:2019-06-18 Revised:2019-09-03 Online:2020-04-15 Published:2020-04-20

Abstract: In order to investigate the prevention and recovery mechanism of ‘Eurotium cristatum Loose Tea’ and its ‘Eurotium cristatum powder’ on mouse lung tissues which were injured by passive smoking, passive cigarette smoking environment (CSE) model on SPF C57BL/6 female mice were established. Mice were fed by 600 mg∙kg-1 Eurotium cristatum tea extract (ECTE) and Eurotium cristatum powder extract (ECPE). Comparing with the CSE model mice, the morphology integrity of lung tissue in passive smoking mice feeding with ECPE and ECTE were significantly protected by observing the pathological slice of lung tissue. The up-regulation levels of IL-6, IL-8, IL-1β, IFN-γ and TNF-α in the serum of mice were inhibited by ELISA analysis. Western blot results show that the expression levels of p-JAK2, p-STAT3, p-JAK2/JAK2, p-STAT3/STAT3 in lung tissues of passive smoking mice fed with ECPE and ECTE were inhibited. These results reveal the prominent protective roles of ECPE and ECTE in the lung injury of passive smoking mice. As a whole, ECPE feeding groups were superior to ECTE feeding groups, while prevention groups were better than treatment groups.

Key words: Eurotium cristatum loose tea, Eurotium cristatum powder, passive smoking, inflammatory cytokines, JAK2/STAT3 signaling pathway

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