Adenosine A2A-receptor agonist polydeoxyribonucleotide promotes gastric ulcer healing in Mongolian gerbils

• Published in: Animal cells and systems Vol. 18; no. 6; pp. 399 - 406
• Main Authors: Jeon, Jung Won, Lee, Joung Il, Shin, Hyun Phil, Cha, Jae Myung, Joo, Kwang Ro, Kim, Sang-Hoon, Ko, Il-Gyu, Jin, Jun-Jang, Kim, Sung-Eun, Kim, Chang-Ju
• Format: Journal Article
• Language: English
• Published: Daejeon Taylor & Francis 01.12.2014; Taylor & Francis Ltd; 한국통합생물학회
• Subjects: Acetic acid; Apoptosis; gastric ulcer; inflammation; Injection; polydeoxyribonucleotide; Ulcers; Vascular endothelial growth factor; 생물학
• ISSN: 1976-8354; 2151-2485
• DOI: 10.1080/19768354.2014.983968

Polydeoxyribonucleotide (PDRN) interacts with the adenosine A 2A -receptor and stimulates vascular endothelial growth factor (VEGF) expression. While it has been indicated that PDRN might accelerate wound healing, its impact on gastric ulcers (GU) is still unknown. We investigated the effects of PDRN on VEGF expression in relation to inflammation and apoptosis in GU by using Mongolian gerbils. GU was induced by injection of acetic acid into the subserosal surface of the stomach. The gerbils in the PDRN-treated groups received daily intraperitoneal injections of PDRN over 2 weeks. Reverse transcriptase-polymerase chain reaction (RT-PCR) for tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, as well as terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) assay, immunohistochemistry for caspase-3, and western blot for VEGF, Bax, and Bcl-2 were conducted. Acetic acid injection induced GU, and VEGF expression in the gastric mucosa was enhanced by GU. PDRN treatment decreased ulcer size and led to overexpression of VEGF in GU. Expression of TNF-α, IL-1β, and IL-6 was increased in GU, and PDRN treatment decreased the expression of these cytokines. The numbers of TUNEL-positive and caspase-3-positive cells were increased by GU, while PDRN reduced these numbers. Induction of GU enhanced the ratio of Bax to Bcl-2, while PDRN diminished this ratio. Overexpression of VEGF and inhibition of inflammation and apoptosis by PDRN may be the underlying mechanisms of PDRN action on GU healing.