Sulfur dioxide derivatives aggravated ovalbumin-induced asthma through targeting TRPV1 and tight junctions

Biosci Biotechnol Biochem. 2023 May 19;87(6):627-637. doi: 10.1093/bbb/zbad039.

Abstract

This study aimed to investigate the effects of sulfur dioxide (SO2) derivatives on asthma induced by ovalbumin (OVA). Sprague Dawley rats were sensitized to and challenged with OVA and SO2 derivatives (NaHSO3 and Na2SO3, 1:3 M/M) to establish 28-day (short-term) and 42-day (long-term) asthma models. Exposure to SO2 derivatives aggravated asthma and hence, promoted lung injury in OVA-induced asthma. In addition, it upregulated the protein expression of TRPV1 and downregulated the expression of tight junctions (TJs). These changes were dose-dependent and were more pronounced in the presence of a high concentration of SO2 derivatives. In vitro, SO2 derivatives also increased the calcium influx and TRPV1 protein expression, and decreased TJ expression. Besides, no significant difference in the TJ expression was found between the WT and TRPV1-/- mice. The underlying mechanism might be related to regulating the effects of TRPV1 and TJs.

Keywords: ovalbumin-induced asthma; sulfur dioxide derivatives; tight junctions; transient receptor potential ion V1.

MeSH terms

  • Animals
  • Asthma* / chemically induced
  • Asthma* / metabolism
  • Disease Models, Animal
  • Lung / metabolism
  • Mice
  • Ovalbumin / adverse effects
  • Rats
  • Rats, Sprague-Dawley
  • Sulfur Dioxide* / adverse effects
  • Sulfur Dioxide* / metabolism
  • TRPV Cation Channels / genetics
  • Tight Junctions

Substances

  • Sulfur Dioxide
  • Ovalbumin
  • TRPV1 protein, mouse
  • TRPV Cation Channels
  • Trpv1 protein, rat