论文部分内容阅读
目的 :研究高良姜素对臭氧所致慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)小鼠气道炎症的影响并探讨其可能机制。方法:32只C57BL/6雄性小鼠随机分为正常对照组、COPD组、COPD+高良姜素组、高良姜素单独给药组。COPD组和COPD+高良姜素组反复给予臭氧吸入,每周3次、1次3 h,共12周;对照组吸入空气。取肺组织切片行苏木素-伊红(hematoxylin-eosin,HE)染色观察气管旁及血管旁炎性细胞浸润;收集支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF),并用酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)法检测BALF中炎症因子水平;实时荧光定量(reverse transcription-polymerase chain reaction,RT-PCR)检测肺组织核转录因子E2相关因子2(nuclear factor-erythroid related factor 2,Nrf-2)及Keap1(Kelch-like ECH-associated protein1,Keap1)mRNA的表达。结果:与正常对照组相比,COPD模型组小鼠气道内炎症细胞浸润程度明显,BALF中炎性细胞亦明显增多;BALF中白介素(interleukin,IL)-6、IL-8及肿瘤坏死因子(tumor necrosis factor,TNF)-α水平显著增高(P<0.05);给予高良姜素可显著缓解炎症严重程度并抑制IL-6、IL-8及TNF-α分泌(P<0.05)。同时高良姜素可使COPD组肺组织Nrf-2水平增高而Keap1未见明显变化。结论:高良姜素可以有效抑制COPD小鼠气道炎症的发生和进展,其机制可能与Nrf-2-Keap1抗氧化系统有关。
Objective: To investigate the effect of galangin on airway inflammation in mice with chronic obstructive pulmonary disease (COPD) induced by ozone and to explore its possible mechanism. Methods: Thirty-two C57BL / 6 male mice were randomly divided into normal control group, COPD group, COPD + galangin group and galangin alone group. The COPD group and the COPD + galangin group were repeatedly given ozone inhalation, 3 times a week, 1 time 3 h, a total of 12 weeks; the control group inhaled air. The lung tissue sections were stained with hematoxylin-eosin (HE) to observe the infiltration of para-tracheal and para-inflammatory cells. The bronchoalveolar lavage fluid (BALF) was collected and analyzed by enzyme-linked immunosorbent assay Immunosorbent assay (ELISA) was used to detect the level of inflammatory cytokines in BALF. The expression of nuclear factor-erythroid related factor 2 (Nrf-2) in lung tissue was detected by reverse transcription-polymerase chain reaction (RT- ) And Keap1 (Kech-like ECH-associated protein1, Keap1) mRNA expression. Results: Compared with the normal control group, the infiltration of inflammatory cells in the airway of the COPD model group was significant and the number of inflammatory cells in the BALF was also significantly increased. The levels of interleukin (IL) -6, IL-8 and tumor necrosis factor (P <0.05). Administration of galangin significantly attenuated the severity of inflammation and inhibited the secretion of IL-6, IL-8 and TNF-α (P <0.05). At the same time galangin can make lung tissue COPD group increased Nrf-2 levels and Keap1 no significant change. CONCLUSION: Galangin can effectively inhibit the occurrence and progression of airway inflammation in COPD mice, and its mechanism may be related to the antioxidant system of Nrf-2-Keap1.