language English
Article 2026 · 0 atıf

The relationship between PDE4 and AQP5 in lung tissue under inflammatory conditions: An experimental study

Bozkurt, Ayse, Bayraktutan, Zafer, Toktay, Erdem, Kara, Adem, Halici, Zekai, Cadirci, Elif

Özet

Objective: This study aimed to examine the relationship between Phosphodiesterase 4 (PDE4) and Aquaporin-5 (AQP5) under Lipopolysaccharide (LPS) induced-inflammatory condition. Methods: Inflammatory Acute lung injury (ALI) was induced by intratracheal LPS (5 mg/kg) administration. Rolipram (intraperitoneal) was used as PDE4 inhibiting agent at three different doses (1, 3 and 5 mg/kg) in rat groups. 24 h after LPS administration lung tissues obtained and following analyses performed. AQP5, Phosphodiesterase 4D (PDE4D), Cyclic adenosine monophosphate (cAMP) levels were evaluated for determination of the relationship between these parameters. Also Interleukin-6 (IL-6), Tumor necrosis factor-alpha (TNF-alpha), Nuclear factor kappa B (NF-kappa B), Mitogen-activated protein kinase (MAPK) levels were evaluated as ALI markers. Results: LPS-induced ALI resulted in increased PDE4 enzyme and inflammatory marker levels (IL-6, TNF-alpha, NF-kappa B and MAPK) and decreased AQP5 and cAMP levels. Inhibition of PDE4 enzyme to increase cAMP levels by Rolipram resulted in increased AQP5 expression and decreased inflammatory condition and in lung tissues. These results were supported by histopathological and immunhistochemical results. Conclusion: The fact that this study observed a decreases PDE4 expression and increases in AQP5 expression upon Rolipram administration might indicate a close relationship of these two parameters in inflammatory lung disease.

Anahtar Kelimeler
ALI AQP5 cAMP LPS PDE4 PHOSPHODIESTERASE-4 INHIBITION AQUAPORIN-5 EXPRESSION INJURY MECHANISMS MODEL CAMP
WoS Kategorileri
Pharmacology & Pharmacy
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES
Yıl
2026
Cilt
217
ISSN
0928-0987
eISSN
1879-0720
DOI
10.1016/j.ejps.2025.107400
WoS UID
WOS:001641224800001
Yayını aç (DOI)