Subchronic inhalation of particulate matter 10 coal dust induces atherosclerosis in the aorta of diabetic and nondiabetic rats

Biomarkers and Genomic Medicine Pub Date : 2014-06-01 DOI:10.1016/j.bgm.2014.03.002

Bambang Setiawan , Nia Kania , Dian Nugrahenny , Nurdiana Nurdiana , Moch. Aris Widodo

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引用次数: 9

Abstract

This study aimed to elucidate whether subchronic inhalation of particulate matter (PM10) coal dust induces atherosclerosis in diabetic rats. A total of 32 male Wistar rats, were randomly divided into eight groups including four nondiabetic groups and four groups of diabetic rats. These rats were exposed to doses of coal dust equal to 0 mg/m³, 6.25 mg/m³, 12.5 mg/m³, or 25 mg/m³ for 1 hour/day for 28 days. Plasma levels of lipid peroxides were determined as thiobarbituric acid reactive substance. The levels of circulating endothelial cells were analyzed histologically. Foam cells formation was analyzed in aorta and tail artery with Oil Red O staining. Analysis of variance test was used to compare all parameters. Nondiabetic rats exposed to coal dust had significantly increased oxidative stress compared to the control group (p < 0.05). Diabetic rats exposed to coal dust at dose of 25 mg/m³ had significantly increased oxidative stress compared to that of control diabetic rats (p < 0.05). The levels of endothelial damage were significantly increased in diabetic rats exposed to coal dust at doses of 6.25 mg/m³ and 12.5 mg/m³ (p < 0.05) compared to control diabetic rats. The foam cell counts were significantly increased in the aorta of nondiabetic rats exposed to coal dust at doses of 6.25 mg/m³ and 25 mg/m³ compared to control rats (p < 0.05), also in the tail artery at dose of 25 mg/m³. The foam cell counts were significantly increased in the aorta of diabetic rats exposed to coal dust at doses of 6.25 mg/m³ and 12.5 mg/m³ than that in control diabetic rats (p < 0.05). Subchronic inhalation of PM10 coal dust induces atherosclerosis through oxidative stress and endothelial damage in aorta of nondiabetic and diabetic rats.

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亚慢性吸入颗粒物10煤尘可诱导糖尿病和非糖尿病大鼠主动脉动脉粥样硬化

本研究旨在阐明亚慢性吸入颗粒物(PM10)煤尘是否诱导糖尿病大鼠动脉粥样硬化。将32只雄性Wistar大鼠随机分为8组，其中4组为非糖尿病大鼠，4组为糖尿病大鼠。这些大鼠分别暴露于0 mg/m3、6.25 mg/m3、12.5 mg/m3或25 mg/m3剂量的煤尘中，每天1小时，持续28天。血浆脂质过氧化物水平测定为硫代巴比妥酸活性物质。组织学分析循环内皮细胞水平。油红O染色观察主动脉和尾动脉泡沫细胞形成情况。采用方差分析检验对各参数进行比较。与对照组相比，暴露于煤尘的非糖尿病大鼠氧化应激显著增加(p <0.05)。25 mg/m3剂量的煤尘对糖尿病大鼠氧化应激的影响显著高于对照组(p <0.05)。暴露于6.25 mg/m3和12.5 mg/m3剂量煤尘的糖尿病大鼠内皮损伤水平显著增加(p <0.05)。与对照大鼠相比，暴露于6.25 mg/m3和25 mg/m3剂量煤尘的非糖尿病大鼠主动脉泡沫细胞计数显著增加(p <0.05)，在25 mg/m3剂量下尾动脉中也有。暴露于6.25 mg/m3和12.5 mg/m3剂量下的糖尿病大鼠主动脉泡沫细胞计数明显高于对照组(p <0.05)。亚慢性吸入PM10煤尘可通过氧化应激和主动脉内皮损伤诱导非糖尿病和糖尿病大鼠动脉粥样硬化。

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Biomarkers and Genomic Medicine

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