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Published on: May 15, 2013
Polydeoxyribonucleotide Attenuates Airway Inflammation Through A2AR Signaling Pathway in PM10-Exposed Mice
Lakkyong Hwang1, Jun-Jang Jin1, Il-Gyu Ko1
1Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea.
Purpose:
Inhalation of air containing high amounts of particular matter (PM) causes various respiratory disorders including asthma, chronic obstructive pulmonary disease, and lung cancer. The changes of expression of inflammatory factors by polydeoxyribonucleotide (PDRN) administration in the PM10-exposed trachea inflammation model were evaluated.
Methods:
PM10 was administered to mouse trachea to induce acute inflammatory damage, and changes in inflammatory factors were observed after administration of PDRN and 3,7-dimethyl-1-propargylxanthine (DMPX) for 3 days daily. Expression of inflammatory cytokines, adenosine A2A receptor (A2AR), protein kinase A (PKA), 3΄,5΄-cyclic adenosine monophosphate responsive element binding protein (CREB) were detected by enzyme-linked immunosorbent assay, immunofluorescence, and western blot assay.
Results:
PM-exposed trachea showed increased tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression, and expression of TNF-α and IL-1β was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased nuclear factor (NF)-κB phosphorylation, and phosphorylation of nuclear factor-kappa B was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased expression of A2AR, but PDRN treatment more enhanced A2AR expression in PM-exposed mice. PKA phosphorylation was not changed and CREP phosphorylation was decreased, however PDRN treatment increased phosphorylation of PKA and CREB in PM-exposed mice. DMPX treatment blocked all the effects of PDRN on PM-exposed mice, demonstrating that the action of PDRN occurs via A2AR.
Conclusion:
PDRN treatment attenuated inflammation in the trachea of the PM10-exposed mice. This improving effect of PDRN can be ascribed to the activation of A2AR through the cAMP-PKA pathway.
Insights
Polydeoxyribonucleotide (PDRN) reduces inflammation in particulate matter (PM)-exposed mouse trachea. PDRN activates the adenosine A2A receptor (A2AR) pathway, mitigating respiratory damage.
Area of Science:
- Environmental Health
- Pulmonology
- Molecular Biology
Background:
- Particulate matter (PM) inhalation triggers respiratory disorders like asthma and lung cancer.
- Understanding the molecular mechanisms of PM-induced inflammation is crucial for developing effective treatments.
Purpose of the Study:
- To evaluate the anti-inflammatory effects of polydeoxyribonucleotide (PDRN) in a mouse model of PM10-induced tracheal inflammation.
- To investigate the role of the adenosine A2A receptor (A2AR) pathway in PDRN's therapeutic action.
Main Methods:
- Acute tracheal inflammation was induced in mice by PM10 exposure.
- Mice received daily PDRN and DMPX treatments for three days.
- Inflammatory markers, A2AR, PKA, and CREB expression/phosphorylation were analyzed using ELISA, immunofluorescence, and Western blot.
Main Results:
- PDRN treatment inhibited the expression of pro-inflammatory cytokines TNF-α and IL-1β in PM-exposed tracheas.
- PDRN suppressed NF-κB phosphorylation and enhanced A2AR expression.
- PDRN increased PKA and CREB phosphorylation, effects blocked by DMPX, confirming A2AR involvement.
Conclusions:
- PDRN effectively attenuates PM10-induced tracheal inflammation in mice.
- The anti-inflammatory mechanism of PDRN involves A2AR activation via the cAMP-PKA pathway.
