AI Article Synopsis
- Glycine, a non-essential amino acid, has been shown to protect against liver ischemia-reperfusion (I/R) injury, though its specific mechanism of action is still unclear.
- In a rabbit study, glycine treatment improved liver blood flow, bile production, and reduced indicators of liver damage compared to the I/R group without glycine.
- The conclusion suggests that glycine helps minimize liver injury by decreasing inflammation and supporting energy production in liver cells during reperfusion.
Article Abstract
Background And Aim: Experimental studies have shown protective effect by the non-essential amino acid glycine to liver ischemia-reperfusion (I/R) injury but the mechanism of action is unknown.
Methods: A rabbit model of hepatic lobar I/R was used. Three groups of animals (n=6) were studied: Sham group (laparotomy alone), ischemia reperfusion (I/R) group (1 h of liver lobar ischemia and 6 h of reperfusion), and a glycine I/R group (intravenous glycine 5 mg/kg prior to the I/R protocol). Systemic and hepatic hemodynamics, degree of liver injury (bile flow, transaminases), hepatic microcirculation, mitochondrial activity (redox state of cytochrome oxidase), bile composition and cytokines (tumor necrosis factor-α and interleukin-8) were measured during the experiment.
Results: Glycine administration increased portal blood flow, bile production, hepatic microcirculation and maintained cytochrome oxidase activity as compared with the I/R group during reperfusion. Glycine also reduced bile lactate surge and stimulated acetoacetate release in bile during reperfusion versus the I/R group. Cytokine levels (tumor necrosis factor-α, interleukin-8) and hepatocellular injury (aspartate aminotransferase and alanine aminotransferase) were significantly reduced by glycine administration.
Conclusion: Intravenous glycine administration reduces liver warm I/R injury by reducing the systemic inflammatory response, and maintaining cellular energy production.
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| http://dx.doi.org/10.1111/j.1440-1746.2010.06323.x | DOI Listing |
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