Exposure to PM2.5 affects blood lipid levels in asthmatic rats through notch signaling pathway

Lipids Health Dis. 2019 Aug 7;18(1):160. doi: 10.1186/s12944-019-1102-8.

Abstract

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.

Keywords: Asthma; Atmospheric PM2.5; Dyslipidemia; Notch signaling pathway.

MeSH terms

  • Animals
  • Asthma / blood*
  • Asthma / chemically induced
  • Asthma / genetics
  • Cholesterol, HDL / blood
  • Cholesterol, LDL / blood
  • Diamines / pharmacology
  • Disease Models, Animal
  • Dyslipidemias / blood*
  • Dyslipidemias / chemically induced
  • Dyslipidemias / genetics
  • Female
  • Gene Expression / drug effects*
  • Lipid Metabolism / drug effects
  • Male
  • Ovalbumin
  • Particulate Matter / administration & dosage*
  • Particulate Matter / antagonists & inhibitors
  • Rats
  • Rats, Wistar
  • Signal Transduction / drug effects*
  • Thiazoles / pharmacology
  • Transcription Factor HES-1 / genetics*
  • Transcription Factor HES-1 / metabolism
  • Triglycerides / blood

Substances

  • 24-diamino-5-phenylthiazole
  • Cholesterol, HDL
  • Cholesterol, LDL
  • Diamines
  • Hes1 protein, rat
  • Particulate Matter
  • Thiazoles
  • Transcription Factor HES-1
  • Triglycerides
  • Ovalbumin