Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup, Jeonbuk 580-185, Republic of Korea.
Food Chem. 2013 May 1;138(1):107-15. doi: 10.1016/j.foodchem.2012.10.026. Epub 2012 Nov 6.
The aim of this study was to investigate the protective effect of 2,3-dehydrosilybin (DHS) against carbon tetrachloride (CCl(4))-induced liver injury in rats. Administration of DHS significantly attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in CCl(4)-treated rats. Moreover, we showed that DHS prevented DNA damage and decreased the protein levels of γ-H2AX, which is a specific DNA damage marker, in CCl(4)-treated rat livers. DHS also markedly increased the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in CCl(4)-treated rat livers. Furthermore, we found that DHS significantly inhibited the production of serum nitric oxide as well as the levels of serum IL-6, IFN-γ, and TNF-α in CCl(4)-treated rats. Additionally, DHS significantly suppressed iNOS expression on the protein levels in CCl(4)-treated rat livers. Collectively, the present study suggests that DHS protects the liver from CCl(4)-induced hepatic damage via antioxidant and anti-inflammatory mechanisms.
本研究旨在探讨 2,3-脱水硅基宾（DHS）对四氯化碳（CCl(4)）诱导的大鼠肝损伤的保护作用。DHS 给药可显著降低 CCl(4)处理大鼠血清中天冬氨酸转氨酶、丙氨酸转氨酶和肝脂质过氧化水平。此外，我们表明 DHS 可防止 CCl(4)处理大鼠肝脏中的 DNA 损伤，并降低 γ-H2AX 的蛋白水平，γ-H2AX 是一种特定的 DNA 损伤标志物。DHS 还可显著增加 CCl(4)处理大鼠肝脏中抗氧化酶的活性，如超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶。此外，我们发现 DHS 可显著抑制 CCl(4)处理大鼠血清中一氧化氮的产生以及血清中 IL-6、IFN-γ 和 TNF-α 的水平。此外，DHS 可显著抑制 CCl(4)处理大鼠肝脏中 iNOS 的蛋白水平表达。综上所述，本研究表明 DHS 通过抗氧化和抗炎机制保护肝脏免受 CCl(4)诱导的肝损伤。
