

Human: Can you summarize the main points of this study?

Abstract
Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress.

Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4 weeks.

Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77 ± 0.34 μg/mg; liquiritin (LQ), 14.55 ± 0.42 μg/mg; and liquiritigenin (LG), 1.34 ± 0.02 μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-α. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-α production was significantly inhibited by licorice.

Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.

Assistant: The main points of this study are that licorice inhibits the development of liver damage, inflammation, and oxidative stress induced by alcohol consumption. Licorice also improves the anti-oxidative activity in the liver and reduces inflammation in response to alcohol. Licorice is thought to have hepatoprotective activity against harmful effects of chronic alcohol consumption.


Human: Can you summarize the main points of this study?

Abstract
Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress.

Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4 weeks.

Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77 ± 0.34 μg/mg; liquiritin (LQ), 14.55 ± 0.42 μg/mg; and liquiritigenin (LG), 1.34 ± 0.02 μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-α. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-α production was significantly inhibited by licorice.

Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.

Assistant: Licorice extract has been demonstrated to be effective in treatment of chronic alcohol-induced liver injury mediated by both inflammation and oxidative damage, including restoration of the antioxidant glutathione level and reducing TNF-α production, as well as inhibition of lipid accumulation in the liver. Studies indicate fermented ethanol-extracted licorice is the most effective type of licorice for treatment of chronic alcohol-induced liver injury, with its major active ingredients being glycyrrhizic acid, licorice flavonoid compounds such as liquiritigenin and liquiritin, which can be standardized to ensure a consistent, reliable dosage. The data from this study provide support for the use of licorice as a promising dietary supplement to treat chronic alcohol-induced liver injury.
Can you summarize the main points of this study?

Abstract
Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress.

Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4 weeks.

Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77 ± 0.34 μg/mg; liquiritin (LQ), 14.55 ± 0.42 μg/mg; and liquiritigenin (LG), 1.34 ± 0.02 μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-α. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-α production was significantly inhibited by licorice.

Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.
user
The main points of this study are that licorice inhibits the development of liver damage, inflammation, and oxidative stress induced by alcohol consumption. Licorice also improves the anti-oxidative activity in the liver and reduces inflammation in response to alcohol. Licorice is thought to have hepatoprotective activity against harmful effects of chronic alcohol consumption.
assistant
Can you summarize the main points of this study?

Abstract
Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress.

Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4 weeks.

Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77 ± 0.34 μg/mg; liquiritin (LQ), 14.55 ± 0.42 μg/mg; and liquiritigenin (LG), 1.34 ± 0.02 μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-α. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-α production was significantly inhibited by licorice.

Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.
user
Licorice extract has been demonstrated to be effective in treatment of chronic alcohol-induced liver injury mediated by both inflammation and oxidative damage, including restoration of the antioxidant glutathione level and reducing TNF-α production, as well as inhibition of lipid accumulation in the liver. Studies indicate fermented ethanol-extracted licorice is the most effective type of licorice for treatment of chronic alcohol-induced liver injury, with its major active ingredients being glycyrrhizic acid, licorice flavonoid compounds such as liquiritigenin and liquiritin, which can be standardized to ensure a consistent, reliable dosage. The data from this study provide support for the use of licorice as a promising dietary supplement to treat chronic alcohol-induced liver injury.
assistant
Can you summarize the main points of this study?

Abstract
Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress.

Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4 weeks.

Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77 ± 0.34 μg/mg; liquiritin (LQ), 14.55 ± 0.42 μg/mg; and liquiritigenin (LG), 1.34 ± 0.02 μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-α. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-α production was significantly inhibited by licorice.

Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.
user
Licorice extract has been demonstrated to be effective in treatment of chronic alcohol-induced liver injury mediated by both inflammation and oxidative damage, including restoration of the antioxidant glutathione level and reducing TNF-α production, as well as inhibition of lipid accumulation in the liver. Studies indicate fermented ethanol-extracted licorice is the most effective type of licorice for treatment of chronic alcohol-induced liver injury, with its major active ingredients being glycyrrhizic acid, licorice flavonoid compounds such as liquiritigenin and liquiritin, which can be standardized to ensure a consistent, reliable dosage. The data from this study provide support for the use of licorice as a promising dietary supplemen
assistant