Asian Pacific Journal of Tropical Medicine (Jan 2018)

Role of NF- κ B signaling pathway in airway inflammation of rats induced by atmospheric PM25

  • Ru-xuan Zhang,
  • Na Li,
  • Jin Jin,
  • Ting-ting Jiang,
  • Yu-wei Wu,
  • Li-ting Zhou

DOI
https://doi.org/10.4103/1995-7645.243108
Journal volume & issue
Vol. 11, no. 13
pp. 40 – 40

Abstract

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Objective: To define the effect of PM2.5 exposure on NF- κ B signaling pathway and airway inflammation, and to reveal the role of NF- K B signaling pathway in airway inflammation induced by atmospheric PM2.5 in rats. Air pollution condition plays an important role in inflammatory response process. Previous studies had suggested that atmospheric PM2.5 was a common environmental problem, influencing almost 98% Southeast Asian populations. Therefore, to study the effect of atmospheric PM2.5 on airway inflammation and its mechanism is of great significance. Methods: Atmospheric PM2.5 from urban traffic trunk roads was collected and prepared into the dry powder. Twenty-four wistar rats (half male and half female) were divided into four groups. Rats in low concentration, middle concentration and high concentration groups were given PM2.5 saline suspension of respectively 1.5, 7.5, 37.5 mg/kg by intratracheal instillation, while rats in control group were given saline. HE stain was used to observe the inflammation reaction of the airway tissue. The levels of TNF-α and IL-1β in rats’ bronchoalveolar lavage fluid (BALF) and serum were measured with ELISA. The expression level of IκB-α protein in the airway of rats was detected by western blot. SPSS 17.0 was used for statistical analysis. Results: The organ coefficient of trachea in the group receiving 1.5 mg/kg PM2.5 was significantly higher than that in control group. In group receiving 7.5 mg/kg PM2.5, the lung tissue inflammation was obvious and the structure damage was mild, while in group of 37.5 mg/kg PM2.5, the airway inflammation was mild and the structure damage was severe. In the serum of rats exposed to the 1.5 mg/kg PM2.5, the level of inflammatory factor TNF-a was significantly lower than that in the control group. The level of TNF-a in BALF of rats exposed to PM2.5 was higher than the control group, and with the exposure dose increasing, the level has decreased. The expression of IκB-α protein in lung tissue of rats exposed to the 1.5 mg/kg PM2.5 has increased than in control group. Conclusion: Atmospheric PM2.5 exposure can damage rats’ airway, affect the level of serum inflammatory factor TNF-α, and the protein expression level of IκB-α. With all considered, the NF-κB signaling pathway may play a role in regulating airway inflammation induced by atmospheric PM2.5.

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