BACKGROUND Epidemiological studies have confirmed atmospheric PM2.5 could affect asthma, and dyslipidemia may be related to pathogenesis of asthma. Recent studies show Notch ligands had lipid combination domains which are responsible for regulating lipid levels. However, the effect of PM2.5 on asthmatic rats' lipid levels and the role of Notch signaling pathway is unclear. METHODS Rats were treat with ovalbumin (OVA) to establish asthma models. Notch signaling pathway inhibitor (DAPT) was injected intraperitoneally. Asthmatic and healthy rats were exposed to different concentrations of PM2.5. Lung tissues were collected and the expression of Hes1 protein was detected by Western Blot. Blood samples were collected to detect the serum lipid levels. RESULTS Hes1 expression levels in healthy and asthma pathway inhibition groups were lower than those in control groups. Compared with control group, rats exposed to PM2.5 in middle and high dose, the levels of TG and TC were decreased. Similar results were observed after exposure to the same concentration of PM2.5 in asthmatic rats. Rats, which were exposed to PM2.5 after being established the asthma model successfully, could exhibit more significant dyslipidemia than those with direct exposure. After Notch signaling pathway inhibited, TC and LDL in asthma pathway inhibition group were lower than those in healthy group. CONCLUSIONS PM2.5 can affect the lipid levels of asthmatic rats through the Notch signaling pathway.

中文翻译：

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暴露于PM2.5会通过Notch信号通路影响哮喘大鼠的血脂水平。

背景技术流行病学研究已经证实，大气中的PM2.5可能会影响哮喘，而血脂异常可能与哮喘的发病机理有关。最近的研究表明，Notch配体具有负责调节脂质水平的脂质结合结构域。然而，尚不清楚PM2.5对哮喘大鼠血脂水平的影响以及Notch信号通路的作用。方法用卵清蛋白（OVA）治疗大鼠以建立哮喘模型。腹膜内注射Notch信号通路抑制剂（DAPT）。哮喘和健康大鼠暴露于不同浓度的PM2.5。收集肺组织，并通过Western Blot检测Hes1蛋白的表达。收集血液样本以检测血清脂质水平。结果健康和哮喘通路抑制组的Hes1表达水平低于对照组。与对照组相比，中高剂量暴露于PM2.5的大鼠TG和TC水平降低。在哮喘大鼠中，暴露于相同浓度的PM2.5后，观察到相似的结果。成功建立哮喘模型后暴露于PM2.5的大鼠比直接暴露的大鼠表现出更大的血脂异常。Notch信号通路被抑制后，哮喘通路抑制组的TC和LDL均低于健康组。结论PM2.5可通过Notch信号通路影响哮喘大鼠的脂质水平。TG和TC水平降低。在哮喘大鼠中，暴露于相同浓度的PM2.5后，观察到相似的结果。成功建立哮喘模型后暴露于PM2.5的大鼠比直接暴露的大鼠表现出更大的血脂异常。Notch信号通路被抑制后，哮喘通路抑制组的TC和LDL均低于健康组。结论PM2.5可通过Notch信号通路影响哮喘大鼠的脂质水平。TG和TC水平降低。在哮喘大鼠中，暴露于相同浓度的PM2.5后，观察到相似的结果。成功建立哮喘模型后暴露于PM2.5的大鼠比直接暴露的大鼠表现出更大的血脂异常。Notch信号通路被抑制后，哮喘通路抑制组的TC和LDL均低于健康组。结论PM2.5可通过Notch信号通路影响哮喘大鼠的脂质水平。哮喘通路抑制组的TC和LDL均低于健康组。结论PM2.5可通过Notch信号通路影响哮喘大鼠的脂质水平。哮喘通路抑制组的TC和LDL均低于健康组。结论PM2.5可通过Notch信号通路影响哮喘大鼠的脂质水平。