摘要
目的研究含氢水对博来霉素(BLM)诱发的小鼠肺纤维化的抑制作用及其机制。方法 54只C57BL/6小鼠随机分为对照(C)组、模型(M)组和氢水干预(H)组,经气管内注射BLM(5 mg/kg)复制肺纤维化模型,分别在建模后7、14和28 d结束实验。分别采用HE和Masson染色检测肺组织炎症反应及肺纤维化程度,肺组织匀浆进行丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性检测;免疫组织化学法检测肺组织核因子-κB p65(NF-κB p65)和肿瘤坏死因子-α(TNF-α)的表达情况。结果含氢水明显减轻BLM所致的肺组织炎症反应和肺纤维化程度;与相同时间点的M组比较,H组的MDA含量降低而SOD活性增高(P<0.05或P<0.01),且肺组织NF-κB p65和TNF-α表达均受到抑制(P<0.05)。结论含氢水可减轻BLM所诱导的小鼠肺纤维化,其机制可能与抑制炎症反应和氧化应激有关。
[Objective] To investigate the inhibition and mechanism of hydrogen water on pulmonary fibrosis of mice induced by Bleomyein (BLM). [Methods] Fifty-two male C57BL/6 mice were randomly divided into three groups; control group (group C), model group (group M) and hydrogen water-treatment group (group H). Group M and group H were induced to pulmonary fibrosis by the method of BLM endotracheal injection , while group C was injected with saline, on 2nd day, group H were given intraperitoneal injection by 6 mL/ (kg·d) mice. All groups were sacrificed on day 7, 14, 28. The sections of the lung were stained by HE and Masson to detect lung tissue alveolitis and pulmonary fibrosis, malonaldehyde (MDA) content and superoxide dismutase (SOD) activity of lung tissue were also detected, immunohistochemical technology was performed to investigate the NF-κB p65 and TNF-α expression in lung specimens. [Results] Alveolitis and the degree of pulmonary fibrosis induced by BLM were significantly attenuated by hydrogen water. The tissue of group H MDA content was decreased while the activity of SOD was evidently enhanced compared with group M at corresponding times (P〈0.05 may be P〈0.01). The expression of NF-κB p65 and TNF-α were significantly lower than those in group M (P 〈0.05). [Conclusion] Hydrogen water attenuates pulmonary fibrosis of mice induced by BLM, the effect of hydrogen water may be associated with the inhibition of the inflammation and oxidative-stress of pulmonary.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2012年第2期29-33,共5页
China Journal of Modern Medicine
基金
泰山医学院青年基金(No:2010ZRQN002)
关键词
含氢水
氧化应激
炎症
肺纤维化
hydrogen water
oxidative-stress
inflammation
pulmonary fibrosis