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PM 暴露诱导 Balb/c 小鼠肝损伤及其复合精油的缓解作用。

Liver injury induced in Balb/c mice by PM exposure and its alleviation by compound essential oils.

机构信息

College of Medical Laboratory, Dalian Medical University, Dalian, 116044, Liaoning Province, People's Republic of China.

Clincal Labortory, Dalian Municipal Friendship Hospital, Dalian, 116001, Liaoning Province, People's Republic of China.

出版信息

Biomed Pharmacother. 2018 Sep;105:590-598. doi: 10.1016/j.biopha.2018.06.010. Epub 2018 Jun 8.

DOI:10.1016/j.biopha.2018.06.010
PMID:29890467
Abstract

Accumulating evidence has suggested a strong link between exposure to air pollution and public health. In particular, inhaled airborne particulate matter <2.5 μm in aerodynamic diameter (PM) can rapidly diffuse from the lungs to the systemic blood circulation and accumulate in the liver. In this study, we used a Balb/c mouse model to investigate liver injury caused by PM inhalation and the anti-inflammatory and antioxidant effects of compound essential oils (CEOs) in alleviating the extent of this injury. The results of serum biochemical and histopathological analyses showed that PM exposure induced inflammatory liver injury, meantime CEOs pretreatment attenuated PM-induced liver inflammatory injury. Western blot and qRT-PCR assays showed that PM increased secretion of cytokines, however CEOs suppressed the production of IL-6 and TNF-α. Furthermore, heme oxygenase-1(HO-1) and superoxide dismutase-1(SOD-1) expression levels showed that PM could trigger oxidative stress-mediated liver injury, whereas CEOs pretreatment might protect against PM-induced liver injury through regulation of the antioxidant system. Molecular analysis showed that the expression of TLR4, a protein which plays a key role in liver health and injury. Results showed that TLR4 was promoted by PM but inhibited by CEOs pretreatment in PM-induced inflammatory liver injury. In addition, PM-promoted secretion of cytokines by activating TLR4/MyD88 pathway, whereas CEOs might alleviate this type of liver inflammation inhibiting the activation of TLR4/MyD88 signaling pathway.

摘要

越来越多的证据表明,暴露于空气污染与公众健康之间存在着密切联系。特别是,吸入的空气动力学直径<2.5μm 的空气悬浮颗粒物(PM)可以迅速从肺部扩散到全身血液循环,并在肝脏中积累。在这项研究中,我们使用 Balb/c 小鼠模型来研究 PM 吸入引起的肝损伤以及复方精油(CEOs)在减轻这种损伤程度方面的抗炎和抗氧化作用。血清生化和组织病理学分析的结果表明,PM 暴露会引起炎症性肝损伤,而 CEOs 预处理可减轻 PM 引起的肝炎症性损伤。Western blot 和 qRT-PCR 检测表明,PM 增加了细胞因子的分泌,而 CEOs 抑制了 IL-6 和 TNF-α的产生。此外,血红素加氧酶-1(HO-1)和超氧化物歧化酶-1(SOD-1)的表达水平表明,PM 可以引发氧化应激介导的肝损伤,而 CEOs 预处理可能通过调节抗氧化系统来预防 PM 引起的肝损伤。分子分析表明,TLR4 蛋白表达在肝脏健康和损伤中起着关键作用。结果表明,PM 促进了 TLR4 的表达,但 CEOs 预处理抑制了 PM 诱导的炎症性肝损伤中的 TLR4 表达。此外,PM 通过激活 TLR4/MyD88 通路促进细胞因子的分泌,而 CEOs 可能通过抑制 TLR4/MyD88 信号通路的激活来减轻这种类型的肝炎症。

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