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1.401331 重庆,重庆医药高等专科学校医学技术学院
2.400016 重庆,重庆医科大学实验教学管理中心
[ 刘方欣, E-mail: dhy12366@126.com LIU Fangxin, E-mail: dhy12366@126.com
收稿:2018-01-29,
修回:2018-03-15,
纸质出版:2018-01
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丁环宇, 段春燕, 高江原, 等. 重庆市交通相关PM2.5短期大剂量暴露对大鼠肺部炎症的影响[J]. 第三军医大学学报, 2018,40(12):1079-1084.
Huanyu DING, Chunyan DUAN, Jiangyuan GAO, et al. Effect of short-term large-dose exposure to traffic-related PM2.5 from Chongqing, China on lung inflammation in rats[J]. Journal of Third Military Medical University, 2018, 40(12): 1079-1084.
丁环宇, 段春燕, 高江原, 等. 重庆市交通相关PM2.5短期大剂量暴露对大鼠肺部炎症的影响[J]. 第三军医大学学报, 2018,40(12):1079-1084. DOI: 10.16016/j.1000-5404.201801234.
Huanyu DING, Chunyan DUAN, Jiangyuan GAO, et al. Effect of short-term large-dose exposure to traffic-related PM2.5 from Chongqing, China on lung inflammation in rats[J]. Journal of Third Military Medical University, 2018, 40(12): 1079-1084. DOI: 10.16016/j.1000-5404.201801234.
目的
2
探讨重庆市交通相关PM2.5短期大剂量暴露对大鼠肺部的损伤作用及对肺部炎症因子表达的影响。
方法
2
2016年9月至2017年2月在重庆市交通要道旁采集交通相关PM2.5样本并制备成PM2.5混悬液。40只健康雌性SD大鼠分为暴露组和对照组(各20只)。暴露组放置于动物全身暴露装置(天津合普,8050CFA)中,雾化吸入0.2 mg/mL PM2.5混悬液,混悬液雾化速度2.5 mL/min,进气流量1 m
3
/min,每天染毒2 h,染毒连续17 d,对照组不做处理。染毒结束后处死大鼠进行支气管肺泡灌洗,灌洗液进行免疫细胞计数并用ELISA法检测炎症因子水平;实时荧光定量PCR检测肺组织炎症因子mRNA的表达;组织学检查大鼠肺部病理改变。
结果
2
交通相关PM2.5染毒后,暴露组大鼠体质量为(229.26±8.14)g,明显低于对照组(268.65±9.37)g(
P
<
0.05)。暴露组大鼠支气管肺泡灌洗液炎症细胞总数、中性粒细胞数、单核/巨噬细胞数、淋巴细胞数分别为(931.10±52.94)×10
6
/L、(148.65±23.13)×10
6
/L、(232.35±21.81)×10
6
/L、(547.20±31.18)×10
6
/L;炎症因子IL-1β、IL-4、IL-6、TNF-α含量分别为(118.13±10.01)、(81.65±5.63)、(135.97±4.93)、(127.17±9.77)pg/mL,均显著高于对照组(
P
<
0.05)。暴露组大鼠肺组织炎症因子IL-1β、IL-4、IL-6 mRNA表达水平分别为(3.06±0.16)、(17.35±0.54)、(7.88±1.01),显著高于对照组;TNF-α mRNA表达水平为(0.83±0.56),显著低于对照组(
P
<
0.05)。肺组织出现充血、淤血,病理切片显示肺内大量炎症细胞浸润。
结论
2
交通相关PM2.5短期大剂量暴露可导致大鼠肺部出现明显炎症反应。
Objective
2
To investigate the effects of short-term high-dose exposure to traffic-related PM2.5 on the expression of inflammatory factors in the lung tissues of rats.
Methods
2
PM2.5 samples were collected at urban roadside locations with a heavy traffic load in Chongqing from September
2016 to February
2017 and prepared into PM2.5 suspension. Forty healthy female SD rats were randomly allocated into 2 equal groups for daily exposure (Animal whole-body exposure device
Tianjin Hepu 8050CFA) to aerosol of 0.2 mg/mL PM2.5 suspension (atomizing velocity 2.5 mL/min
intake flow rate 1 m
3
/min
for 2 h per day) for 17 consecutive days (exposure group
n
=20) or with no treatment (control group
n
=20). The rats were sacrificed at the end of the exposure
and bronchoalveolar lavage fluid (BALF) was collected for measurement of the levels of interleukin-1β (IL-1β)
IL-4
IL-6 and tumor necrosis factor-α (TNF-α) using enzyme-linked immunosorbent assay (ELISA). The expression of IL-1β
IL-4
IL-6 and TNF-α at mRNA level in the lung tissue of the rats were detected using qPCR
and pathological changes in the lungs were examined.
Results
2
The rats with exposure to traffic-related PM2.5 showed a significant reduction in body weight as compared with the control rats (229.26±8.14 g
vs
268.65±9.37 g
P
<
0.05). PM2.5 exposure
result
2
ed in significantly increased counts of total inflammatory cells [(931.10±52.94)×10
6
/L
]
neutrophils [(148.65±23.13)×10
6
/L
]
monocytes/macrophages [(232.35± 21.81)×10
6
/L
]
and lymphocytes [(547.20±31.18)×10
6
/L
]
and elevated levels of IL-1β [(118.13±10.01) pg/mL
]
IL-4 [(81.65±5.63) pg/mL
]
IL-6 [(135.97±4.93) pg/mL
]
and TNF-α (127.17± 9.77) pg/mL in the BALF compared with control group (
P
<
0.05). The exposure also caused significantly increased mRNA expression of IL-1β (3.06±0.16)
IL-4 (17.35±0.54) and IL-6 (7.88±1.01) and lowered expression of TNF-α mRNA (0.83±0.56) in the lu
ng tissue (
P
<
0.05). Pathological examination revealed massive lung inflammatory cell infiltration in the lungs of the exposed rats.
Conclusion
2
Short-term high-dose exposure to traffic-related PM2.5 induces obvious inflammation in the lungs of rats.
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