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Abstract
ObjectiveTo assess alterations in perfusion and liver function in the concanavalin A (ConA)-induced mouse model of acute liver failure (ALF) using two magnetic resonance imaging (MRI)-based methods: dynamic contrast-enhanced MRI (DCE-MRI) with Gd-EOB-DTPA contrast agent and arterial spin labelling (ASL).Materials and methodsBALB/c mice were studied using a 9.4 T MRI system. The IntraGateFLASHTM and FAIR-EPI pulse sequences were used for optimum mouse abdomen imaging.ResultsThe average perfusion values for the liver of the control and ConA group were equal to 245 ± 20 and 200 ± 32 ml/min/100 g (p = 0.008, respectively). DCE-MRI showed that the time to the peak of the image enhancement was 6.14 ± 1.07 min and 9.72 ± 1.69 min in the control and ConA group (p < 0.001, respectively), while the rate of the contrast wash-out in the control and ConA group was 0.037 ± 0.008 and 0.021 ± 0.008 min−1 (p = 0.004, respectively). These results were consistent with hepatocyte injury in the ConA-treated mice as confirmed by histopathological staining.ConclusionsBoth the ASL and DCE-MRI techniques represent a reliable methodology to assess alterations in liver perfusion and hepatocyte integrity in murine hepatitis.
Highlights
Acute liver failure is a disease associated with high mortality and multiorgan dysfunction [1]
concanavalin A (ConA)–induced hepatitis involves cooperative activation of natural killer T (NKT) with conventional T cells and Kupffer cells and IL-4, TNF-α- and IFN-γ-mediated liver inflammation in mice with subsequent development of hepatocellular apoptosis and necrosis [10,11,12] that eventually results in endothelium disintegration and necrosis of hepatocytes [10]
Numerous foci of necrosis scattered throughout the parenchyma in the livers of the ConA group were observed
Summary
Acute liver failure is a disease associated with high mortality and multiorgan dysfunction [1]. ALF is associated with a primary liver dysfunction, activation of pro-inflammatory responses including proinflammatory cytokines, acute phase proteins [4], and activation of liver sinusoidal endothelial cells (LSEC), Kupffer cells and recruitment of immune cells [5]. ALF invariably leads to the loss of hepatocyte integrity as mirrored by the elevated levels of the liver specific enzymes [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] in blood [6]. It influences the functional state of the liver leading to haemodynamic disturbances, inappropriate vasodilatation and reduction of perfusion [7,8,9]. ConA–induced hepatitis involves cooperative activation of natural killer T (NKT) with conventional T cells and Kupffer cells and IL-4-, TNF-α- and IFN-γ-mediated liver inflammation in mice with subsequent development of hepatocellular apoptosis and necrosis [10,11,12] that eventually results in endothelium disintegration and necrosis of hepatocytes [10]
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