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空气中臭氧毒性水平对大鼠炎症反应的局部和全身影响

Local and Systemic Influence of Toxic Levels of Airborne Ozone on The Inflammatory Response in Rats.

作者信息

Chmielewska-Krzesińska Małgorzata, Wąsowicz Krzysztof

机构信息

Department of Pathophysiology, Forensic Veterinary Medicine and Administration, Faculty of Veterinary Medicine, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland.

出版信息

J Vet Res. 2021 Oct 6;65(4):513-517. doi: 10.2478/jvetres-2021-0051. eCollection 2021 Dec.

DOI:10.2478/jvetres-2021-0051
PMID:35112007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8775738/
Abstract

INTRODUCTION

Ozone is not harmful itself; however, it directly oxidises biomolecules and produces radical-dependent cytotoxicity. Exposure to ozone is by inhalation and therefore the lungs develop the main anti-inflammatory response, while ozone has an indirect impact on the other organs. This study investigated the local and systemic effects of the ozone-associated inflammatory response.

MATERIAL AND METHODS

Three groups each of 5 Wistar Han rats aged 6 months were exposed for 2h to airborne ozone at 0.5 ppm and a fourth identical group were unexposed controls. Sacrifice was at 3h after exposure for control rats and one experimental group and at 24 h and 48 h for the others. Lung and liver samples were evaluated for changes in expression of transforming growth factor beta 1, anti-inflammatory interleukin 10, pro-inflammatory tumour necrosis factor alpha and interleukin 1 beta and two nuclear factor kappa-light-chain-enhancer of B cells subunit genes. Total RNA was isolated from the samples in spin columns and cDNA was synthesised in an RT-PCR. Expression levels were compared to those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and analysed statistically.

RESULTS

All variables changed non-linearly over time comparing experimental groups to the control. Conspicuous expression changes in the subunit genes and cytokines were observed in both evaluated organs.

CONCLUSION

Locally and systemically, inflammation responses to ozone inhalation include regulation of certain genes' expression. The mechanisms are unalike in lungs and liver but ozone exerts a similar effect in both organs. A broader range of variables influential on ozone response should be studied in the future.

摘要

引言

臭氧本身并无危害;然而,它会直接氧化生物分子并产生自由基依赖性细胞毒性。臭氧通过吸入进入人体,因此肺部会产生主要的抗炎反应,而臭氧对其他器官有间接影响。本研究调查了与臭氧相关的炎症反应的局部和全身影响。

材料与方法

将三组,每组5只6个月大的Wistar Han大鼠暴露于0.5 ppm的空气中臭氧中2小时,第四组相同的大鼠作为未暴露的对照组。对照组大鼠和一个实验组在暴露后3小时处死,其他组在24小时和48小时处死。对肺和肝样本进行评估,以检测转化生长因子β1、抗炎性白细胞介素10、促炎性肿瘤坏死因子α和白细胞介素1β的表达变化以及两个B细胞亚基基因的核因子κB轻链增强子。从样本中在旋转柱中分离总RNA,并在逆转录聚合酶链反应(RT-PCR)中合成cDNA。将表达水平与甘油醛-3-磷酸脱氢酶(GAPDH)的表达水平进行比较,并进行统计学分析。

结果

与对照组相比,所有变量随时间呈非线性变化。在两个评估器官中均观察到亚基基因和细胞因子的明显表达变化。

结论

局部和全身而言,吸入臭氧后的炎症反应包括某些基因表达的调节。肺和肝中的机制不同,但臭氧在两个器官中都发挥了类似的作用。未来应研究更广泛的影响臭氧反应的变量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec8/8775738/92ac85c55450/jvetres-65-513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec8/8775738/c2373fbb95df/jvetres-65-513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec8/8775738/92ac85c55450/jvetres-65-513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec8/8775738/c2373fbb95df/jvetres-65-513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cec8/8775738/92ac85c55450/jvetres-65-513-g002.jpg

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本文引用的文献

1
Prophylaxis and therapeutic potential of ozone in buiatrics: Current knowledge.臭氧在儿科的预防和治疗潜力:当前知识
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2
Suppression of antigen presentation by IL-10.白细胞介素-10对抗抗原呈递的抑制作用。
Curr Opin Immunol. 2015 Jun;34:22-7. doi: 10.1016/j.coi.2014.12.009. Epub 2015 Jan 16.
3
Molecular mechanisms underpinning laser printer and photocopier induced symptoms, including chronic fatigue syndrome and respiratory tract hyperresponsiveness: pharmacological treatment with cinnamon and hydrogen.
激光打印机和复印机诱发症状(包括慢性疲劳综合征和呼吸道高反应性)的分子机制:肉桂和氢气的药物治疗
Neuro Endocrinol Lett. 2013;34(8):723-37.
4
Chronic exposure to emissions from photocopiers in copy shops causes oxidative stress and systematic inflammation among photocopier operators in India.在印度,复印店的复印机排放物会导致复印机操作人员长期暴露在其中,从而引发氧化应激和系统性炎症。
Environ Health. 2013 Sep 11;12(1):78. doi: 10.1186/1476-069X-12-78.
5
Ozone oxidative postconditioning ameliorates joint damage and decreases pro-inflammatory cytokine levels and oxidative stress in PG/PS-induced arthritis in rats.臭氧氧化后处理可改善关节损伤,降低 PG/PS 诱导的关节炎大鼠促炎细胞因子水平和氧化应激。
Eur J Pharmacol. 2013 Aug 15;714(1-3):318-24. doi: 10.1016/j.ejphar.2013.07.034. Epub 2013 Jul 31.
6
Long-term improvement in refractory headache following ozone therapy.臭氧治疗后难治性头痛的长期改善。
J Altern Complement Med. 2013 May;19(5):453-8. doi: 10.1089/acm.2012.0273. Epub 2012 Dec 7.
7
Primer-BLAST: a tool to design target-specific primers for polymerase chain reaction.Primer-BLAST:一种用于设计聚合酶链反应(PCR)目标特异性引物的工具。
BMC Bioinformatics. 2012 Jun 18;13:134. doi: 10.1186/1471-2105-13-134.
8
TGF-β and NF-κB signal pathway cross-talk is mediated through TAK1 and SMAD7 in a subset of head and neck cancers.TGF-β 和 NF-κB 信号通路的串扰是通过 TAK1 和 SMAD7 在一部分头颈部癌症中介导的。
Oncogene. 2013 Mar 21;32(12):1549-59. doi: 10.1038/onc.2012.171. Epub 2012 May 28.
9
Regulation and function of NF-kappaB transcription factors in the immune system.NF-κB转录因子在免疫系统中的调控与功能
Annu Rev Immunol. 2009;27:693-733. doi: 10.1146/annurev.immunol.021908.132641.
10
Effect of aqueous ozone on the NF-kappaB system.臭氧水溶液对核因子-κB系统的影响。
J Dent Res. 2007 May;86(5):451-6. doi: 10.1177/154405910708600512.