Abstract
BackgroundEpidemiological 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.MethodsRats 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.ResultsHes1 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.ConclusionsPM2.5 can affect the lipid levels of asthmatic rats through the Notch signaling pathway.
Highlights
Epidemiological studies have confirmed atmospheric PM2.5 could affect asthma, and dyslipidemia may be related to pathogenesis of asthma
Exposure to PM2.5 can cause the accumulation of triglycerides (TG) and total cholesterol (TC) in the serum, which may lead to dyslipidemia by triggering inflammation [1]
The asthmatic rats had behaved shortness of Evaluation of notch signaling pathway inhibition To confirm that DAPT has inhibitory effects on Notch signaling pathway in rats, we performed western blots and found that the expression level of hes1 was significantly lower in the healthy pathway inhibition (HI) and asthma pathway inhibition (AI) groups than other three control groups (p < 0.05, Fig. 3a-b)
Summary
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. The effect of PM2.5 on asthmatic rats’ lipid levels and the role of Notch signaling pathway is unclear. Fine specific matter (PM2.5) refers to particles with an aerodynamically equivalent diameter ≤ 2.5 μm. Researches had indicated that PM2.5 was a risk factor for the development of many diseases, including metabolic syndrome. Exposure to PM2.5 can cause the accumulation of triglycerides (TG) and total cholesterol (TC) in the serum, which may lead to dyslipidemia by triggering inflammation [1]. Zheng point out PM2.5 exposure causes lung and vascular abnormalities, possibly related to oxidative stress, endoplasmic reticulum stress and inflammatory
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