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Adenosine A2A Receptor Agonist Polydeoxyribonucleotide Alleviates Interstitial Cystitis-Induced Voiding Dysfunction by Suppressing Inflammation and Apoptosis in Rats

Authors Ko IG, Jin JJ, Hwang L, Kim SH, Kim CJ, Won KY, Na YG, Kim KH, Kim SJ

Received 21 October 2020

Accepted for publication 24 December 2020

Published 15 February 2021 Volume 2021:14 Pages 367—378

DOI https://doi.org/10.2147/JIR.S287346

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Professor Ning Quan


Il-Gyu Ko,1 Jun-Jang Jin,1 Lakkyong Hwang,1 Sang-Hoon Kim,1 Chang-Ju Kim,1 Kyu Yeoun Won,2 Yong Gil Na,3 Khae Hawn Kim,3 Su Jin Kim4

1Department of Physiology, College of Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea; 2Department of Pathology, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, 05278, Korea; 3Department of Urology, Chungnam National University Sejong Hospital, College of Medicine, Chungnam National University, Sejong-si, 30099, Republic of Korea; 4Department of Urology, Yonsei University Wonju College of Medicine, Wonju, 26426, Republic of Korea

Correspondence: Su Jin Kim
Department of Urology, Yonsei University Wonju College of Medicine, 20 Ilsanro, Wonju, Gangwon-do, 26426, Republic of Korea
Tel +82-10-3287-0615
Email hygeiasujin@naver.com

Background: Interstitial cystitis (IC) is a chronic disorder that indicates bladder-related pain or discomfort. Patients with IC often experience urination problems, such as urinary frequency and urgency, along with pain or discomfort in the bladder area. Therefore, new treatments based on IC etiology are needed. Polydeoxyribonucleotide (PDRN) is a biologic agonist of the adenosine A2A receptor, and PDRN has anti-inflammatory effect and inhibits apoptosis. In the current study, the effect of PDRN on cyclophosphamide-induced IC animal model was investigated using rats.
Methodology: To induce the IC animal model, 75 mg/kg of cyclophosphamide was injected intraperitoneally once every 3 days for 10 days. The rats in the PDRN-treated groups were intraperitoneally injected with 0.5 mL physiological saline containing 8 mg/kg PDRN, once a day for 10 days after IC induction.
Results: Induction of IC by cyclophosphamide injection caused voiding dysfunction, bladder edema, and histological damage. Cyclophosphamide injection increased secretion of pro-inflammatory cytokines and enhanced apoptosis. In contrast, PDRN treatment alleviated voiding dysfunction, bladder edema, and histological damage. Secretion of pro-inflammatory cytokines and expressions of apoptotic factors were suppressed by PDRN treatment. These changes indicate that treatment with PDRN improves voiding function by ultimately promoting the repair of damaged bladder tissue.
Conclusion: The conclusion of this experiment suggests the possibility that PDRN could be used as an effective therapeutic agent for IC.

Keywords: interstitial cystitis, adenosine A2A receptor, polydeoxyribonucleotide, voiding function, inflammation, apoptosis

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