Relaxin as an Additional Protective Substance in Preserving and Reperfusion Solution for Liver Transplantation, Shown in a Model of Isolated Perfused Rat Liver

Abstract

Reperfusion injury is a problem in organ transplantation. Relaxin causes vessel dilation and inhibition of platelet and mast cell activation. The study investigates the protective effect of relaxin on liver tissue against cell damage during organ preservation and reperfusion. Liver transplantation was simulated in a model of isolated perfused rat liver. Relaxin was applicated during reperfusion and/or preservation. To quantify cell damage, we examined the perfusate for malonyldialdehyde (MDA) and myeloperoxidase activity (MPO), and liver tissue underwent immunohistochemical study. Relaxin as an additional substance in preserving/reperfusion solution decreases MPO and MDA levels in the perfusate and immunohistochemical study. Relaxin seems to have a protective effect against cell damage in ischemia and reperfusion injury.

Relaxin receptors in hepatic stellate cells and cirrhotic liver

“…Porcine relaxin treatment caused morphological changes in rat perisinusoidal liver cells, and dilation of the sinusoids [14]. Relaxin had protective effects against ischemia and reperfusion damage in perfused rat liver [37]. In a recent study, 20-fold overexpression of mouse relaxin for 4 months in a transgenic mouse model resulted in increased liver weight and hydroxyproline in males but not females [26].…”

Cardiovascular effects of relaxin: from basic science to clinical therapy

“…[37][38][39][40][41][42][43][44][45][46][47] In a rat stroke model, relaxin reduces infarct size in a NO-dependent manner, 48 and decreases leukocyte recruitment to areas of inflammation. These effects may involve increased expression and activity of nitric oxide synthase (NOs).…”

Relaxin as a natural agent for vascular health

“…Of note, in this study, the injured heart also appears to up-regulate the production and release of endogenous RLX, providing support to the view that RLX is a cardiac hormone (Taylor and Clark 1994) and may have paracrine effects against cardiac ischemic injury and dysfunction (Dschietzig et al 2001). As occurs in the heart, RLX has been shown to protect against IR-induced injury in other organs, such as the liver (Boehnert et al 2005), the small bowel (Masini et al 2006), the pancreas (Cosen-Binker et al 2006) and the brain (Wilson et al 2006). In all these studies, direct or indirect evidence is provided that the protection afforded by RLX relies on its effects on the endothelium and often involve endogenous NO generation.…”