Glabridin Ameliorates Alcohol-Caused Liver Damage by Reducing Oxidative Stress and Inflammation via p38 MAPK/Nrf2/NF-κB Pathway.
Mengyao WangFeng ZhangJie ZhouKe GongShasha ChenXinran ZhuMengxue ZhangYajun DuanChenzhong LiaoJihong HanZequn YinPublished in: Nutrients (2023)
Licorice is a traditional and versatile herbal medicine and food. Glabridin (Gla) is a kind of isoflavone extracted from the licorice root, which has anti-obesity, anti-atherosclerotic, and antioxidative effects. Alcoholic liver disease (ALD) is a widespread liver disease induced by chronic alcohol consumption. However, studies demonstrating the effect of Gla on ALD are rare. The research explored the positive effect of Gla in C57BL/6J mice fed by the Lieber-DeCarli ethanol mice diet and HepG2 cells treated with ethanol. Gla alleviated ethanol-induced liver injury, including reducing liver vacuolation and lipid accumulation. The serum levels of inflammatory cytokines were decreased in the Gla-treated mice. The reactive oxygen species and apoptosis levels were attenuated and antioxidant enzyme activity levels were restored in ethanol-induced mice by Gla treatment. In vitro, Gla reduced ethanol-induced cytotoxicity, nuclear factor kappa B (NF-κB) nuclear translocation, and enhanced nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation. Anisomycin (an agonist of p38 MAPK) eliminated the positive role of Gla on ethanol-caused oxidative stress and inflammation. On the whole, Gla can alleviate alcoholic liver damage via the p38 MAPK/Nrf2/NF-κB pathway and may be used as a novel health product or drug to potentially alleviate ALD.
Keyphrases
- oxidative stress
- nuclear factor
- diabetic rats
- toll like receptor
- high fat diet induced
- dna damage
- induced apoptosis
- ischemia reperfusion injury
- alcohol consumption
- drug induced
- weight loss
- liver injury
- type diabetes
- insulin resistance
- signaling pathway
- metabolic syndrome
- public health
- physical activity
- mental health
- body mass index
- risk assessment
- immune response
- high glucose
- human health
- cell death
- mouse model
- endothelial cells
- inflammatory response
- adipose tissue
- climate change
- case control
- electronic health record
- lps induced