文献类型：期刊文献

中文题名：阿魏酸拮抗大气PM2.5对大鼠肺的损伤作用

英文题名：Protective Effect of Ferulic Acid on Lung Injury Induced by PM2.5 in Rats

作者：周艳丽[1];劳文艳[1,2];阮研硕[3];毕婷婷[1];陈世杰[1];赵晓红[1,2]

第一作者：周艳丽

通讯作者：Zhao, Xiaohong

机构：[1]北京联合大学功能食品科学技术研究院,北京100191;[2]北京联合大学生物活性物质与功能食品北京市重点实验室,北京100191;[3]中国医学科学院医学实验动物研究所,北京协和医学院比较医学中心,北京100021

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院功能食品科学技术研究院

年份：2017

卷号：38

期号：1

起止页码：244-251

中文期刊名：食品科学

外文期刊名：Food Science

收录：CSTPCD;;EI(收录号：20171003409465);Scopus;北大核心:【北大核心2014】；CSCD:【CSCD_E2017_2018】；

基金：中国营养学会营养科研基金-帝斯曼专项(2015-030(CNS-DSM));北京联合大学生物活性物质与功能食品北京市重点实验室开放课题(Zk70201501)

语种：中文

中文关键词：阿魏酸;PM2.5;大鼠;肺损伤;拮抗作用

外文关键词：ferulic acid; PM2.5; rats; lung injury; protective effect

摘要：探讨阿魏酸干预北京市大气PM2.5对大鼠肺的损伤作用,为预防和控制PM2.5造成的健康危害提供基础数据。通过建立空白对照组、不同剂量PM2.5(1.5、6.0、24.0 mg/kg)染毒组及相应阿魏酸保护组,取肺组织进行苏木精-伊红染色观察组织形态学变化;收集肺泡灌洗液(bronchoalveolar lavage fluid,BALF)进行炎性细胞计数,并测定乳酸脱氢酶、碱性磷酸酶和酸性磷酸酶活力;测定血液上清液丙二醛(methane dicarboxylic aldehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)活力、8-羟基脱氧鸟苷(8-hydroxy-2-deoxyguanosine,8-OHd G)含量;测定肺组织匀浆上清液免疫球蛋白E(immunoglobulin E,Ig E)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素(interleukin,IL)-4、IL-8、核转录因子-κB(nuclear factorkappa B,NF-κB)含量及Toll样受体(Toll-like receptor,TLR)-4含量。结果显示,PM2.5染毒能够造成大鼠肺组织不同程度病理性改变;BALF中炎性细胞密度增加,且具有剂量依赖关系,6.0 mg/kg PM2.5中剂量组,损伤作用最明显;阿魏酸剂量为38.8 mg/kg时可以抑制这种改变。剂量为38.8 mg/kg的阿魏酸可以抑制PM2.5染毒引起的血清中MDA含量升高、SOD活力降低和8-OHd G含量升高。PM2.5染毒后,Ig E、TNF-α、IL-4和TLR-4含量增加,阿魏酸预处理可以抑制其增加。因此,PM2.5对大鼠肺部造成明显的氧化损伤和炎性损伤,阿魏酸能够减轻该损伤作用,可能是通过抑制Toll样受体通路减轻PM2.5诱导的炎症反应。
The protective effect of ferulic acid (FA) on rat lung injury induced by PM2.5 in Beijing was studied in the present investigation aiming to provide basic information for the prevention and control of health hazard caused by PM2.5. Rats were treated with PM2.5 at different concentrations (1.5, 6.0, and 24.0 mg/kg) with and without pre-administration of FA.Histopathological changes of lung tissue were detected by hematoxylin-eosin (HE) staining. Bronchoalveolar lavage fluid (BALF) was collected to count the number of inflammatory cells and detect the expressions of lactate dehydrogenase (LDH),alkaline phosphatase (AKP) and acidic phosphatase (ACP). Blood supernatant was used for measuring the levels of methanedicarboxylic aldehyde (MDA), superoxide dismutase (SOD) and 8-hydroxy-2-deoxyguanosine (8-OHdG). The homogenatesupernatant of lung tissue was collected for detecting the concentrations of immunoglobulin E (IgE), tumor necrosisfactor-alpha (TNF-α), interleukin-4 (IL-4), interleukin-8 (IL-8), nuclear factor-kappa B (NF-κB) and Toll-like receptor-4(TLR-4). The results showed that PM2.5 exposure caused a dose-dependent pathological change of lung tissue and anincrease in inflammatory cells in BALF. PM2.5 at 6.0 mg/kg caused the greatest damage. FA (38.8 mg/kg) prevented theincrease in the expressions of MDA and 8-OHdG as well as the concentrations of IgE, TNF-α, IL-4 and TLR-4, and the decrease in SOD activity induced by PM2.5. Therefore, PM2.5 can cause significant oxidative damage and inflammatory injury to the lung tissue in rats.These damages can be prevented by pre-administration of FA potentially through inhibition of Toll-like receptor signaling.