Find in Library

Background: Mitochondrial plays a vital role in regulating obesity and related comorbidity. Targeting mitochondrial function could be a potent therapeutic approach to inhibit metabolic-related diseases like obesity, liver disease. Prolonged use of existing drug moieties demonstrated severe adverse effects. Methods: We apply Ucp1-A-GFP immortalized reporter cell lines and HEK293T cell lines to evaluate cell viability, mitochondrial ATP production, and the in-silico model. Results: We found Glycyrrhizin, an HMGB1 (high mobility group box 1) inhibitor, plays a significant role in modulating mitochondrial function against obesity. At the cellular level, the adipocytes treated with Glycyrrhizin have increased mitochondrial function. Further analysis shows that compared with the control group, the cells in the treatment group contain more mitochondria. Glycyrrhizin demonstrated a nontoxic effect on the HEK293T cell line, upregulating mitochondrial DNA and reducing mitochondrial ATP production levels. In-silico study exhibited drug-protein interaction and binding side with UCP1. Conclusion: Glycyrrhizin improves mitochondrial function that would be an effective drug candidate to treat metabolic diseases and obesity-related diseases. Further investigation will require both the human and animal models to reveal new insight into the mechanism against obesity, metabolic diseases or mitochondrial dysfunction-related diseases.