Abstract
Organoprotective effects of noble gases are subject of current research. One important field of interest is the effect of noble gases on hepatic regenerative capacity. For the noble gas argon, promising studies demonstrated remarkable experimental effects in neuronal and renal cells. The aim of this study was to investigate the effects of argon on the regenerative capacity of the liver after ischemia/reperfusion injury (IRI). Male, Sprague-Dawley rats underwent hepatic IRI by clamping of the hepatic artery. Expression of hepatoproliferative genes (HGF, IL-1β, IL-6, TNF), cell cycle markers (BrdU, TUNEL, Ki-67), and liver enzymes (ALT, AST, Bilirubin, LDH) were assessed 3, 36, and 96 h after IRI. Expression of IL-1β and IL-6 was significantly higher after argon inhalation after 36 h (IL-1β 5.0 vs. 8.7 fold, p = 0.001; IL-6 9.6 vs. 19.1 fold, p = 0.05). Ki-67 was higher in the control group compared to the argon group after 36 h (214.0 vs. 38.7 positive cells/1000 hepatocytes, p = 0.045). Serum levels of AST and ALT did not differ significantly between groups. Our data indicate that argon inhalation has detrimental effects on liver regeneration after IRI as measured by elevated levels of the proinflammatory cytokines IL-1β and IL-6 after 36 h. In line with these results, Ki-67 is decreased in the argon group, indicating a negative effect on liver regeneration in argon inhalation.
Highlights
Ischemia-reperfusion injury (IRI) is an undesirable consequence of organ transplantation and frequently occurs in other clinical settings such as major liver surgery or circulatory shock after resuscitation [1,2,3]
The aim of this study was to investigate the effects of argon on the regenerative capacity of the liver after ischemia/reperfusion injury (IRI)
Based on the current evidence about the organoprotective effects of argon in renal and neuronal cells, this noble gas appeared to be a promising candidate to reduce hepatic IRI [17,18,19,20,21,22]. This is the first study investigating the effect of argon inhalation on hepatic IRI by measuring apoptosis, regenerative capacity, the modulation of the inflammatory response, and the effect on laboratory parameters
Summary
Ischemia-reperfusion injury (IRI) is an undesirable consequence of organ transplantation and frequently occurs in other clinical settings such as major liver surgery or circulatory shock after resuscitation [1,2,3]. It is one of the most important determinants of organ dysfunction (i.e., liver failure) and determines short- and long-term morbidity and mortality after liver resection and transplantation [4,5,6]. The use of noble gases has gained attention. Previous studies showed some remarkable cytoprotective effects of noble gases in different clinical settings.
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