紫苏干预COPD系统性炎症的大鼠模型研究

发布时间：2018-02-23 12:48

本文关键词： 慢性阻塞性肺疾病紫苏香烟烟雾系统性炎症　出处：《天然产物研究与开发》2017年08期 　论文类型：期刊论文

【摘要】：为揭示导入紫苏基因的新型烟草的生物学效应,将54只清洁级雄性SD大鼠随机分为健康对照组(CK)、普通烟草组(GT)和新型烟草组(NT),采用烟雾熏吸法构建COPD模型。对血清进行ELISA分析显示,香烟烟雾染毒56 d能诱发COPD大鼠的系统性炎症反应;但与GT组相比,NT组的CRP、IL-8以及TNF-α水平显著降低(P0.05)。取肝和脾组织进行IHC检测发现,COPD大鼠的NF-κB p65表达水平明显升高,且GT组与NT组脾组织间的差异显著(P0.05)。结果表明,导入紫苏基因的新型烟草能够抑制大鼠吸烟相关性COPD的全身性炎症反应,干预肺外组织NF-κB的过度活化,延缓疾病的进程。
[Abstract]:In order to reveal the biological effects of new tobacco introduced perilla gene, Fifty-four clean male Sprague-Dawley rats were randomly divided into healthy control group, common tobacco group and new tobacco group. The COPD model was established by smoke fumigation. The ELISA analysis of serum was performed. The systemic inflammatory response of COPD rats was induced by cigarette smoke exposure for 56 days, but the levels of IL-8 and TNF- 伪 in NT group were significantly lower than those in GT group. The expression of NF- 魏 B p65 in liver and spleen tissues was significantly higher than that in GT group, and the expression level of NF- 魏 B p65 in liver and spleen tissues was significantly increased after exposure to cigarette smoke for 56 days. The difference between GT group and NT group was significant (P 0.05). The results showed that the new tobacco introduced perilla gene could inhibit the systemic inflammation of smoking-related COPD in rats, interfere with the excessive activation of NF- 魏 B in extrapulmonary tissue, and delay the progression of the disease.
【作者单位】：山西大学生命科学学院;
【基金】：山西省回国留学人员科研资助项目(2013-024) 山西省重点研发计划(社会发展)(201603D321002)
【分类号】：R285.5;R-332

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