Suppressive effects of mead acid supplementation on acute liver damage derived from green tea extract

Abstract

〈Background〉 We reported on the characteristics of green tea extract (GTE)-induced hepatotoxicity in rats. Using this model, we explored the inhibitory effects of n-9 PUFA, mead acid (MA), by dietary supplementation. 〈Methods〉 7-week-old male Sprague-Dawley rats received a single intraperitoneal injection of 200 mg/kg GTE, serum and liver were collected 24, 48 hrs, and 7 days after the GTE injection. The control or 4.8% MA diets was given from one week before GTE injection to sacrifice. Control diet + saline, 4.8% MA diet + saline, control diet + GTE, and 4.8% MA diet + GTE groups were set. Serum biomarkers of hepatotoxicity [aspartate aminotransferase (AST), alanine aminotransferase (ALT)], liver histopathology, and immunohistochemistry of apoptosis (γH2A.X), oxidative stress (8-nitroguanosine) and hypoxia [hypoxia inducible factor (HIF)-1α] were examined. Fatty acid in serum and liver tissue of the control diet + saline and 4.8% MA diet+ saline groups were analyzed. 〈Results〉 In the control diet + GTE group, AST and ALT levels increased. Centrilobular hepatocellular necrosis was seen 24 and 48 hrs after GTE exposure. Furthermore, the levels of these changes decreased in the MA diet group. In the control diet + GTE group, γH2A.X, 8-nitroguanosine, and HIF-1α-positive hepatocytes appeared and peaked at 48 hrs. The level of these changes reduced by MA diet feeding. MA composition in the serum and liver significantly increased in the MA diet group, compared to the control diet group. 〈Conclusion〉The levels of GTE-induced liver damage, such as serum biomarkers, histology, and immunohistochemistry for hepatotoxicity were inhibited by MA diet feeding. This effect may be related to suppression of cell death via the pathway of oxidative stress and hypoxia in the liver.