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AcSDKP对大鼠矽肺c-jun氨基末端激酶通路活化的调节作用
  • ISSN号:1001-9391
  • 期刊名称:中华劳动卫生职业病杂志
  • 时间:2013
  • 页码:335-340
  • 分类:R361.3[医药卫生—病理学;医药卫生—基础医学]
  • 作者机构:[1]华北理工大学附属唐山市工人医院呼吸内科,唐山063000, [2]华北理工大学基础医学院病理学系,唐山063000
  • 相关基金:国家自然科学基金面上项目(编号:81072254); 唐山市医疗卫生创新人才培养项目(编号:14130275B); 华北理工大学杰出青年基金项目(编号:JP201507)
  • 相关项目:AcSDKP抗矽肺纤维化作用的比较蛋白质组学研究
中文摘要:

目的探讨硫氧环蛋白过氧化物酶1(Prx-1)对矽肺大鼠肺组织纤维化的影响。方法健康成年雄性SD大鼠按抽签法随机分为4组:对照组(生理盐水)、SiO_2组(50mg/只)、SiO_2+空慢病毒组(空慢病毒滴度5×10^7TU)和SiO_2+-Prx-1慢病毒组(Prx-1慢病毒滴度5×10^7TU),每组10只。气管内注入SiO_2和慢病毒,造模后饲养4周。HE染色观察肺组织形态学变化、免疫组化法检测α-SMA表达,Western blot法检测肺组织Prx-1及Ⅰ和Ⅲ型胶原水平、硫代巴比妥酸法检测丙二醛(MDA)水平。结果① SiO_2+Prx-1慢病毒组的Prx-1蛋白表达明显高于SiO_2+空慢病毒组,差异有统计学意义(P〈0.05);②对照组大鼠肺组织结构基本正常;SiO_2组和SiO_2+空慢病毒组大鼠肺泡壁增厚或断裂,细胞性矽结节形成;但SiO_2+Prx-1慢病毒组大鼠肺泡壁变薄,矽结节体积减小;③与对照组比较,SiO_2组α-SMA、Ⅰ型胶原蛋白、Ⅲ型胶原蛋白及MDA表达水平均明显增加,差异有统计学意义(P〈0.05)。SiO_2+空慢病毒组的α-SMA、Ⅰ和Ⅲ型胶原蛋白及MDA表达水平与SiO_2组无明显区别;但与SiO_2+空慢病毒组比较,SiO_2+Prx-1慢病毒组的α-SMA、Ⅰ型胶原蛋白、Ⅲ型胶原蛋白及MDA表达水平明显下降,差异有统计学意义(P〈0.05)。结论 Prx-1能够抑制SiO_2诱导的肺组织纤维化,这一作用与降低ROS、抑制肌成纤维细胞分化有关。

英文摘要:

Objective To study the effect of peroxredoxin-1 ( Prx-1 ) on SiO2-induced puhnonary fibrosis in rats. Methods Healthy adult male SD rats were divided into four groups randomly:control( saline, n=10) , SiO2 group (50 mg/rat, n = 10), SiO2 + empty lentivirus group( empty lentivirus :5 × 10^7 TU, n = 10) and SiO2 + Prx-1 lentivir- us group (Prx-1 lentivirus :5 × 10^7 TU,n = 10). SiO: and lentivirus were given by tracheal injection and then all an- imals were observed for four weeks. HE staining was used to observe pulmonary morphological changes and immu- nohistochemical staining was used to detect α-SMA expression. Western blot was used to measure expressions of Prx-1, collagen type I and re,and thiobarbituric acid assay was used to detect malondialdehyde(MDA) content. Results The expression of Prx-1 protein in SiO2 + Prx-1 lentivirus group was significantly higher than that in SiO2 + empty lentivirus group [ (0.45 ± 0.05 ) vs (0. 35 ± 0.05 ), P 〈 0.05 ]. HE staining showed that the structure of the lung tissue of the control group was normal, and the alveolar wall was thin. There were lung tissue structural damage, alveolar wall thickening or fracture, and the formation of cellular silicon nodules in SiO2 group and SiO2 + empty lentivirus group. However, the alveolar wall became thinner and the size of silicon nodules became smallerin SiO2 + Prx-I lentivirus group. Compared with control, expressions of α-SMA, collagen type I and Ill, and MDA content in SiO2 group significantly increased [ ( 0. 40 ± 0. 16 ) vs ( 6.60 ± 0.70 ), ( 0. 34 ±0. 05 ) vs ( 0. 45 ±0. 05 ), (0. 18 ±0. 03)vs(0.34 ±0. 06) and(2.31 ±0.35)vs(3.46 ±0.44) ,P 〈0. 05]. There were no differences in the levels of α-SMA, collagen type I and m, and MDA content between SiO2 group and SiO2 + lentivirus group. Compared with SiO2 + empty lentivirus group, levels of α-SMA, collagen type I and m, and MDA content in SiO2 + Prx-1 lentivirus group marke

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期刊信息
  • 《中华劳动卫生职业病杂志》
  • 中国科技核心期刊
  • 主管单位:中国科协
  • 主办单位:中华医学会
  • 主编:
  • 地址:天津河东区华越道6号
  • 邮编:300011
  • 邮箱:cjoh1983@163.com
  • 电话:022-24333581
  • 国际标准刊号:ISSN:1001-9391
  • 国内统一刊号:ISSN:12-1094/R
  • 邮发代号:6-50
  • 获奖情况:
  • 2000年中华医学会优秀期刊银奖,2000年天津市优秀期刊奖,2001中华预防医学会优秀期刊一等奖
  • 国内外数据库收录:
  • 美国化学文摘(网络版),波兰哥白尼索引,荷兰文摘与引文数据库,美国生物医学检索系统,日本日本科学技术振兴机构数据库,中国中国科技核心期刊,中国北大核心期刊(2004版),中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2000版)
  • 被引量:16727