Abstract
Acute liver failure (ALF) is a life-threatening disorder of liver function. Kynurenic acid (KYNA), a tryptophan metabolite formed along the kynurenine metabolic pathway, possesses anti-inflammatory and antioxidant properties. Its presence in food and its potential role in the digestive system was recently reported. The aim of this study was to define the effect of KYNA on liver failure. The Wistar rat model of thioacetamide-induced liver injury was used. Morphological and biochemical analyses as well as the measurement of KYNA content in liver and hepatoprotective herbal remedies were conducted. The significant attenuation of morphological disturbances and aspartate and alanine transaminase activities, decrease of myeloperoxidase and tumor necrosis factor-α, and elevation of interleukin-10 levels indicating the protective effect of KYNA in thioacetamide (TAA) - induced liver injury were discovered. In conclusion, the hepatoprotective role of KYNA in an animal model of liver failure was documented and the use of KYNA in the treatment of ALF was suggested.
Highlights
Acute liver failure (ALF), the essence of which lies in acute massive hepatocyte necrosis, may lead to shock, coagulation disorders, encephalopathies, brain oedema, renal failure, infection, and development of multiple organ failures [1]
The aim of this study was to examine the effect of Kynurenic acid (KYNA) in the rat mode of acute liver injury induced by thioacetamide (TAA)
TAA administration resulted in a marked increase in the levels of aspartate transaminase (AST) and alanine transaminase (ALT) to 316.3 ± 59.3 U/L and 90.2 ± 12.9 U/L, respectively
Summary
Acute liver failure (ALF), the essence of which lies in acute massive hepatocyte necrosis, may lead to shock, coagulation disorders, encephalopathies, brain oedema, renal failure, infection, and development of multiple organ failures [1]. Treatment of ALF is based on adjunctive therapy carried out until the proper functioning of the liver is reestablished. For whom donors are unavailable, the support with bioartificial liver and complex critical care protocols are considered as lifesaving bridge therapy. The bridge measures lead to survival when the liver function spontaneously recovers [5, 6]. The mechanism of spontaneous restoration of liver function after acute failure is under debate [7]. There is a continuing need for other treatment options and protective measures decreasing the risk of liver failure
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