Int Neurourol J.  2020 Nov;24(Suppl 2):88-95. 10.5213/inj.2040430.215.

Protective Effect of Polydeoxyribonucleotide Against CCl4-Induced Acute Liver Injury in Mice

Affiliations
  • 1Department of Surgery, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea
  • 2Department of Pathology, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea

Abstract

Purpose
Polydeoxyribonucleotide (PDRN) is a substance known to suppress inflammation and accelerate wound healing. In this experiment, the effect of PDRN treatment on carbon tetrachloride (CCl4)-evoked acute liver injury (ALI) was investigated using mice.
Methods
We analyzed the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and conducted hematoxylin and eosin staining in accompany with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Western blot analysis was also conducted to assess the expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, adenosine A2A receptor, Bcl-2-associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2). The mice were received intraperitoneal injection of 10-mL/kg CCl4, 4 times, once every 2 days. The mice in the PDRN treatment groups received intraperitoneal injection of 200-μL distilled water comprising each concentration of PDRN for 7 days starting 1 day after first CCl4 injection.
Results
ALT and AST concentrations in the serum were reduced and TNF-α, IL-1β, and IL-6 expressions were decreased by PDRN injection in CCl4-evoked ALI mice. PDRN injection suppressed Bax versus Bcl-2 ratio and reduced the percentage of TUNE-positive cells in CCl4-evoked ALI mice. PDRN injection overexpressed adenosine A2A receptor in CCl4-evoked ALI mice.
Conclusions
The therapeutic efficacy of PDRN also can be expected for CCl4-evoked acute urogenital injury in addition to ALI. The current research suggests that PDRN may be used for the therapeutic agent of CCl4-evoked ALI.

Keyword

Acute liver injury; Carbon tetrachloride; Adenosine A receptor; Polydeoxyribonucleotide; Proinflammatory cytokines; Apoptosis
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