第一临床医学院机构知识库

Institutional Repository, First Clinical School

 

兰州大学机构库  > 第一临床医学院  > 期刊论文
题名: Inhibitory effects of codonopsis pilosula polysaccharides on the deterioration of impaired phagocytosis of alveolar macrophage induced by fine particulate matter in chronic obstructive pulmonary disease mice
其他题名: 党参多糖对细颗粒物所致慢性阻塞性肺疾病小鼠肺泡巨噬细胞吞噬功能障碍加剧的抑制作用
作者: Chu, X; Liu, X J; Qiu, J M; Zeng, X L; Bao, H R
收录类别: PubMed ; MEDLINE ; CSCD
出版日期: 2016-04-12
刊名: 中华医学杂志
卷号: 96, 期号:14, 页码:1134-1138
期刊主办单位: 中华医学会
出版地: BEIJING
中文摘要: 目的探讨党参多糖(CPP)对细颗粒物(PM2.5)所致慢性阻塞性肺疾病(慢阻肺)小鼠肺泡巨噬细胞(AM)吞噬功能障碍加剧的抑制作用。方法60只雄性BALB/c小鼠按随机数字表法随机分为正常对照组、慢阻肺组、PM2.5组、PM2.5慢阻肺组、CPP慢阻肺组、CPP + PM2.5慢阻肺组各10只。采用烟草烟雾暴露法建立慢阻肺模型,PM2.5组、PM2.5慢阻肺组、CPP + PM2.5慢阻肺组给予PM2.5(770 μg/m~3)雾化吸入90 d,CPP慢阻肺组、CPP + PM2.5慢阻肺组给予CPP(300 mg/kg)灌胃90 d,余各组等体积生理盐水灌胃。造模结束后即采用小鼠无创体描箱检测肺功能,吸气峰流速(PIF)和呼气峰流速(PEF);处死小鼠取肺组织,行病理学检查并测定平均肺泡间隔(MLI);采用不连续密度梯度离心法分离AM,流式细胞术检测AM吞噬荧光素异硫氰酸酯标记的大肠杆菌(FITC- E. coli)的能力,用平均荧光强度(MFI)、吞噬E. coli阳性细胞百分比(吞噬%)表示。分别用菲罗啉比色法、硫代巴比妥酸比色法、改良Hafeman法检测肺组织匀浆总抗氧化能力(TAC)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-PX)水平。结果正常对照组、慢阻肺组、PM2.5组、PM2.5慢阻肺组、 CPP慢阻肺组、CPP + PM2.5慢阻肺组MFI和吞噬% 分别为:10 267 ± 1 358、4 817 ± 399、8 469 ± 240、 3 176±501、5 886 ±516、4 067 ±453和(69.0 ±5.4)%、(30.7 ±3.0)%、(51.5 ±2.4)%、(20.4 ± 3.5)% 、(38.7 ±2.6)% 、(28.7 ±4.3)%;慢阻肺组和PM2.5组MFI和吞噬%均显著低于正常对照组,且PM2.5慢阻肺组均显著低于慢阻肺组,CPP慢阻肺组、CPP + PM2.5慢阻肺组分别显著高于慢阻肺组、PM2.5慢阻肺组(均P< 0.01) 。 各组TAC和GSH-PX分别为:(17.99 ± 0.09)、 (6.83 ± 0.36)、(13.84 ±1.12)、(3.61 ±0.29) 、(8.80 ±0.26)、(5.43 ±0.30)U/mg蛋白和(84 3 ±5.7)、(46.5 ± 2.6)、(62.0 ±2.2)、(32.4 ± 3.8)、(53.4 ±4.0)、(42.4 ±4.0) U/mg;慢阻肺组和PM2.5组TAC、 GSH-PX均显著低于正常对照组,且PM2.5慢阻肺组均显著低于慢阻肺组,CPP慢阻肺组、CPP + PM2.5慢阻肺组分别显著高于慢阻肺组、PM2.5慢阻肺组(均P < 0.01)。各组MDA分别为:(1.74 ± 0.37)、(2.73 ±0.22)、(2.01 ±0.13)、(3.55 ±0.33)、 (2.22 ±0.28)、(2.72 ± 0.44) nmol/mg蛋白;慢阻肺组和PM2.5组MDA均显著高于正常对照组,且PM2.5慢阻肺组显著高于慢阻肺组;CPP慢阻肺组、CPP + PM2.5慢阻肺组分别显著低于慢阻肺组、PM2.5慢阻肺组(均P <0.05)。相关性分析:基础状态下、PM2.5干预、CPP干预及PM2.5联合CPP干预后,慢阻肺小鼠MFI和吞噬%与TAC、GSH水平均呈正相关,与MDA水平呈负相关。结论PM2.5加剧慢阻肺小鼠AM吞噬功能障碍,恶化氧化应激;CPP对此有抑制作用,其机制与抗氧化作用密切相关。
英文摘要: OBJECTIVE: To investigate the inhibitory effects of codonopsis pilosula polysaccharides (CPP) on the deterioration of impaired phagocytosis of alveolar macrophage (AM) induced by fine particulate matter with a mean aerodynamic diameter ≤2.5 mum (PM2.5) in chronic obstructive pulmonary disease (COPD) mice.METHODS: Sixty BALB/c male mice were randomly divided into control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group. COPD mice were established using exposure of cigarette smoking. Meanwhile PM2.5 group, PM2.5 COPD group and CPP+ PM2.5 COPD group were exposed to PM2.5 (770 mug/m(3)) for 90 days. CPP COPD group and CPP+ PM2.5 COPD group were fed with CPP (300 mg/kg) for 90 days whilst other groups were fed with isovolumetric saline. After the models were established, mice peak inspiratory flow (PIF) and peak expiratory flow (PEF) were measured by noninvasive body plethysmograph and lung histopathology and mean linear intercept (MLI) were observed. AMs were isolated from lung tissue by discontinuous density gradient centrifugation. Mean fluorescence intensity (MFI) and the ability of AM phagocytosing flurescein isothiocyanate-labeled Escherichia coli (FITC-E.coli) (AM%) were detected by flow cytometry. Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry. Malondialdehyde (MDA) was measured by thiobarbiturieacid colorimetry and glutathione peroxidase (GSH-PX) by improved Hafeman colorimetry.RESULTS: MFI in control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group were 10 267±1 358, 4 817±399, 8 469±240, 3 176±501, 5 886±516 and 4 067±453. AM% in each group were (69.0±5.4)%, (30.7±3.0)%, (51.5±2.4)%, (20.4±3.5)%, (38.7±2.6)% and (28.7±4.3)%. MFI and AM% in COPD group and PM2.5 group were decreased than those in control group while those in PM2.5 COPD group were lower than in COPD group (all P<0.01). Comparing to COPD group and PM2.5 COPD group respectively, MFI and AM% in CPP COPD group and CPP + PM2.5 COPD group were increased (all P<0.01). TAC and GSH-PX in each group were (17.99±0.09), (6.83±0.36), (13.84±1.12), (3.61±0.29), (8.80±0.26), (5.43±0.30) U/mg protein and (84.3±5.7), (46.5±2.6), (62.0±2.2), (32.4±3.8), (53.4±4.0), (42.4±4.0) U/mg. TAC and GSH-PX in COPD group and PM2.5 group were lower than those from control group while those from PM2.5 COPD group were decreased than in COPD group (all P<0.01). Comparing to COPD group and PM2.5 COPD group, TAC and GSH-PX in CPP COPD group and CPP+ PM2.5 COPD group were increased respectively (all P<0.01). MDA in each group were (1.74±0.37), (2.73±0.22), (2.01±0.13), (3.55±0.33), (2.22±0.28) and (2.72±0.44) nmol/mg protein. MDA in COPD group and PM2.5 group were higher than that from control group while that from PM2.5 COPD group was higher than in COPD group; MDA in CPP COPD group and CPP+ PM2.5 COPD group were respectively decreased than those in COPD group and PM2.5 COPD group (all P<0.05). Positive correlations were existed between MFI, AM% and TAC, GSH-PX, while negative correlations were existed between MFI, AM% and MDA in COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group.CONCLUSIONS: PM2.5 further impaired the defective phagocytosing capacity of AM and exacerbated oxidative stress in COPD mice. CPP can inhibit these effects. The protection of CPP may be closely related to its antioxidative effects.
关键词: 肺疾病,慢性阻塞性 ; 党参多糖 ; 细颗粒物 ; 巨噬细胞,肺泡 ; 氧化性应激 ; 小鼠
作者部门: Department of Gerontal Respiratory Medicine, the First Hospital of Lanzhou University, Lanzhou 730000, China.
文章类型: Article
所属项目编号: 甘肃省中医药科学技术研究课题 ; 甘肃省科技支撑计划
所属项目名称: 甘肃省科技支撑计划
项目资助者: GSSTD
语种: 中文
DOI: 10.3760/cma.j.issn.0376-2491.2016.14.016
ISSN号: 0376-2491
CSCD记录号: CSCD:5668825
PM记录号: 27095785
IR记录号: 27095785
第一机构:
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.lzu.edu.cn/handle/262010/178640
Appears in Collections:第一临床医学院_期刊论文

Files in This Item:

There are no files associated with this item.


Recommended Citation:
Chu, X,Liu, X J,Qiu, J M,et al. Inhibitory effects of codonopsis pilosula polysaccharides on the deterioration of impaired phagocytosis of alveolar macrophage induced by fine particulate matter in chronic obstructive pulmonary disease mice[J]. Zhonghua yi xue za zhi,2016,96(14):1134-1138.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Altmetrics Score
 
Google Scholar
Similar articles in Google Scholar
[Chu, X]'s Articles
[Liu, X J]'s Articles
[Qiu, J M]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Chu, X]‘s Articles
[Liu, X J]‘s Articles
[Qiu, J M]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Email:
Passwd
验 证:
换一张
Have you forgotten your password? Log In
Copyright © 2007-2017  兰州大学 - Feedback
Powered by CSpace