曲尼司特抗大鼠肺纤维化的作用及机制

中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (7): 754-759.

曲尼司特抗大鼠肺纤维化的作用及机制

徐红蕾, 金旭如, 陈少贤

温州医学院第一附属医院呼吸内科, 温州325000, 浙江

收稿日期:2009-03-09 修回日期:2009-06-30 出版日期:2009-07-26 发布日期:2020-10-30
作者简介:徐红蕾, 女, 硕士, 副教授, 硕导, 研究方向:间质性肺疾病。Tel:13566262606 　E-mail:xfhl2000@yuhoo.com.cn

Inhibitory effects and mechanisms of tranilast on pulmonary fibrosis in rats

XU Hong-lei, JIN Xu-ru, CHEN Shao-xian

First Hospital of Wenzhou Medical College, Respiratory Medicine, Wenzhou 325000, Zhejiang, China

Received:2009-03-09 Revised:2009-06-30 Online:2009-07-26 Published:2020-10-30

摘要/Abstract

摘要： 目的:探讨曲尼司特对肺纤维化的治疗作用及机制。方法:48 只Sprague-Dauley 大鼠随机分为正常对照组(N 组)、肺纤维化模型组(M 组) 和曲尼司特治疗组(Q 组) 各16 只, 分别在14、28 d处死8 只, 每组大鼠分别采用HE 染色、Masson 染色行肺泡炎、肺纤维化程度分级。采用免疫组化法检测肺组织NF-κB;荧光定量PCR 技术测定TGF-β₁ mRNA 表达;样本碱水解法测定羟脯氨酸(HYP);DTNB 法测定超氧化物歧化酶(SOD);硫代巴比妥酸法测定丙二醛(MDA)。结果:M 组的肺泡炎及肺纤维化程度及HYP 含量、NF-κB、转化生长因子-β₁ (TGF-β₁) mRNA 及MDA 含量均较N组显著升高(P<0.01)。Q 组大鼠肺泡炎及肺纤维化程度及HYP 含量、NF-κB、TGF-β₁ mRNA MDA含量均较M 组显著降低(P<0.01)。结论:曲尼司特可能是通过抑制氧自由基生成而下调了NF-κB 的活性, 从而抑制了TGF-β mRNA 的表达而发挥抗肺纤维化作用。

关键词: 肺纤维化, NF-κB, 转化生长因子-β₁, 氧自由基, 曲尼司特

Abstract: AIM: To explore the inhibitory effects and mechanisms of tranilast on bleomycin-induced pulmonary fibrosis in rats.METHODS: Fourty-eight Sprague-Dauley rats were randomly divided into normal control group (Group N, n=16), pulmonary fibrosis model group (Group M, n=16), and tranilast treatment group (Group Q, n=16).Eight rats in each group were sacrificed on days 14 and 28 following the day of animal model establishment.The degree of airsacculitis and pulmonary fibrosis were detected by HE andMasson staining in each group rats.The concentrations of NF-κB, expressions of TGF-β₁ mRNA and concentrations of Hydroxyproline (HYP), SOD and MDA in lung tissue were detected by the immunohistochemical method, fluorescent quantitative PCR, allaki hydrolysis, DTNB and thiobarbituric acid method in each group, respectively.RESULTS: The concentrations of NF-κB, expressions of TGF-β₁ mRNA and concentrations of HYP, SOD andMDA in lung tissue were significantly higher in GroupM than in Group N (P<0.01) and was significantly lower in Q group than inM group (P<0.01).CONCLUSION: The anti-pulmonary fibrosis effect of tranilast may be achieved through inhibited the generation of oxygen free radicals and thus decreased the activity of NF-κB, thereby inhibited TGF-β mRNA expression.

Key words: pulmonary fibrosis, NF-κB, TGF-β₁, oxygen free radical, tranilast

中图分类号:

R563.9
R976

徐红蕾, 金旭如, 陈少贤. 曲尼司特抗大鼠肺纤维化的作用及机制[J]. 中国临床药理学与治疗学, 2009, 14(7): 754-759.

XU Hong-lei, JIN Xu-ru, CHEN Shao-xian. Inhibitory effects and mechanisms of tranilast on pulmonary fibrosis in rats[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2009, 14(7): 754-759.

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