研究了绿茶多酚（Green tea polyphenol,GTP）对被动吸烟致小鼠肺部氧化应激损伤的干预作用,并探讨其可能机制。将40只KM雌性小鼠随机分成正常对照C组、被动吸烟模型M组、100βmg·kg-1 GTP1组、200βmg·kg-1 GTP2组,每组10只。实验12周结束后处死小鼠,测定其肺质量及血清氧化应激炎症水平;采用荧光定量PCR测定白细胞介素6（IL-6）、白细胞介素33（IL-33）、肿瘤坏死因子-α（TNF-α）和白细胞介素1β（IL-1β）基因表达水平。研究结果表明,与M组相比,灌喂GTP后使得小鼠生存质量、肺形态有明显改观,显著提高小鼠血清T-SOD及GSH-Px活力,显著降低MDA、IL-6、TNF-α表达水平,显著抑制IL-6、IL-33、TNF-α及IL-1β炎性相关基因的表达,灌胃200βmg·kg-1 GTP比100βmg·kg-1的GTP作用更加显著。研究发现,GTP可能通过抑制炎性细胞因子表达水平、提高抗氧化能力来保护肺部组织形态与结构的完整,保护被动吸烟对肺部的损害。
The objective of the study is to investigate the intervention effects of green tea polyphenols (GTP) on oxidative stress induced by passive smoking in mice lung and its possible mechanisms. Forty healthy Kunming mice (female) were randomly divided into 4 groups including normal control group (C), passive smoking model group (M), GTP treated group 1 (GTP1, 100βmg·kg-1) and GTP treated group 2 (GTP2, 200βmg·kg-1) respectively (n=10). All mice were killed after treating with GTP for 12 weeks. The morphology and quality of lung, the oxidative stress of serum and inflammatory level were determined. The mRNA expression levels of inflammation-related genes including interleukin 6 (IL-6), interleukin 33 (IL-33), tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) were measured by fluorescence quantitative PCR. Compared to M group, the life quality and pulmonary morphology of mice in GTP1 and GTP2 were significantly improved, and T-SOD and GSH-Px activities in serum were also significantly enhanced. But MDA, IL-6 and TNF-α levels in serum were decreased significantly. The mRNA expressions of IL-6, IL-33, TNF-α and IL-1β were also declined in GTP groups, which were clearly dose-dependent. These results showed that GTP could protect lung against damage of passive smoking and remain the integrity of lung tissues by inhibiting inflammatory cytokine expression and improving the antioxidant capacity.
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