白茶对烟雾诱导的小鼠慢性阻塞性肺病的改善研究

60只ICR小鼠随机等分成正常对照组、模型组、寿眉组、白牡丹组、白毫银针组和表没食子儿茶素没食子酸酯（EGCG）组。通过烟熏法建立小鼠慢性阻塞性肺病（Chronic obstructive pulmonary,COPD）模型,3个等级的白茶水提物和EGCG通过灌胃给予药物,5周后处死,收集血浆、支气管肺泡灌洗液、肺组织和肝组织,测定肺组织病理学变化和各样品的生化指标,研究白茶对小鼠COPD的改善作用及机制。结果显示：（1）模型组肺组织出现大量炎性浸润与杯状细胞化生等病理损伤,白茶提取物和EGCG处理均能明显改善肺组织病理性损伤,白毫银针效果最佳;（2）模型组出现明显的氧化应激和炎症反应,丙二醛（MDA）、白介素-6（IL-6）与肿瘤坏死因子-α（TNF-α）水平显著升高,超氧化物歧化酶（SOD）活性显著下降,白茶提取物和EGCG处理均能显著降低MDA、IL-6与TNF-α水平并上调SOD活性;（3）模型组血浆一氧化氮（NO）水平和肺组织髓过氧化物酶（MPO）活性显著升高,在支气管肺泡灌洗液和肺组织中NO水平降低,白茶提取物和EGCG组均能改善NO失调,降低MPO活性;（4）白茶提取物和EGCG均能上调COPD小鼠单磷酸腺苷依赖的蛋白激酶（AMPK）磷酸化水平的下降;上述处理过程中均未见白茶提取物和EGCG对小鼠的肝毒性。综上,白茶提取物能够通过抗氧化、抗炎和调节NO失常来明显改善香烟烟雾诱导的小鼠COPD。

Improvement of White Tea on Cigarette Smoke-induced Chronic Obstructive Pulmonary Disease in Mice

Sixty ICR mice were randomly divided into normal control group, model control group, Shoumei group, Baimudan group, Baihaoyinzhen group and epigallocatechin gallate group (EGCG). Chronic obstructive pulmonary (COPD) model of mice was established by smoking method. Three kinds of white tea water extracts and epigallocatechin gallate (EGCG) were administered by intragastric administration and sacrificed after five weeks, and plasma, bronchoalveolar lavage fluid, lung tissue and liver tissue were collected to determine the pathological changes of lung tissue and the biochemical indicators of each group. The improvement effect and mechanism of white tea on COPD in mice were shown as follows: (1) In the model group, a large amount of pathological damage such as inflammatory infiltration and goblet cell metaplasia appeared in the lung tissue. Both white tea extracts and EGCG treatment could obviously improve the pathological damage of the lung tissue, and the Baihaoyinzhen extract had the best effect. (2) Model group showed obvious oxidative stress and inflammation. The levels of malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) increased significantly, and the activity of superoxide dismutase (SOD) decreased significantly. Both white tea extracts and EGCG treatment could significantly reduce MDA, IL-6 and TNF-α levels and up-regulate SOD activity. (3) The nitric oxide (NO) level of plasma and myeloperoxidase (MPO) activity of lung tissues increased significantly in model group, on the contrary NO level decreased in BALF and lung tissues. Both the white tea extracts and the EGCG could improve NO disorders and reduced MPO activity. (4) Both white tea extracts and EGCG could improve the decline of phosphorylation level of adenosine monophosphate-dependent protein kinase (AMPK) in COPD mice. No liver toxicity of white tea extracts or EGCG was found in mice under treatments. In summary, white tea extracts could obviously improve cigarette smoke-induced COPD in mice by anti-oxidation, anti-inflammatory and regulating NO abnormalities.