Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study
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 e...
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| Format: | Article |
| Language: | English |
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Elsevier
2022-05-01
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| Series: | Journal of Saudi Chemical Society |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1319610322000369 |
| _version_ | 1811257753458442240 |
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| author | Md. Reyad-ul-Ferdous Mohnad Abdalla Yongfeng Song |
| author_facet | Md. Reyad-ul-Ferdous Mohnad Abdalla Yongfeng Song |
| author_sort | Md. Reyad-ul-Ferdous |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T18:02:23Z |
| format | Article |
| id | doaj.art-72d15865c1fd41a3aa48b6b677cfb7b7 |
| institution | Directory Open Access Journal |
| issn | 1319-6103 |
| language | English |
| last_indexed | 2024-04-12T18:02:23Z |
| publishDate | 2022-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Saudi Chemical Society |
| spelling | doaj.art-72d15865c1fd41a3aa48b6b677cfb7b72022-12-22T03:22:07ZengElsevierJournal of Saudi Chemical Society1319-61032022-05-01263101454Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico studyMd. Reyad-ul-Ferdous0Mohnad Abdalla1Yongfeng Song2Department of Endocrinology and Metabolism, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China; Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong, 250021, China; Shandong Institute of Endocrinology & Metabolism, Shandong, China; Shandong Institute of Endocrinology & Metabolism, Shandong Academy of Clinical Medicine, Jinan, Shandong, 250021, China.; Corresponding authors at: Department of Endocrinology and Metabolism, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China (Md. Reyad-ul-Ferdous); Department of Endocrinology and Metabolism, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong, China (Y. Song).Key Laboratory of Chemical Biology (Ministry of Education), Department of Pharmaceutics, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province 250012, PR ChinaDepartment of Endocrinology and Metabolism, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China; Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong, 250021, China; Department of Endocrinology and Metabolism, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong, China; Shandong Institute of Endocrinology & Metabolism, Shandong, China; Shandong Institute of Endocrinology & Metabolism, Shandong Academy of Clinical Medicine, Jinan, Shandong, 250021, China.; Corresponding authors at: Department of Endocrinology and Metabolism, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China (Md. Reyad-ul-Ferdous); Department of Endocrinology and Metabolism, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong, China (Y. Song).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.http://www.sciencedirect.com/science/article/pii/S1319610322000369ObesityMitochondrial ATP productionMitochondrial DNA quantificationCell viabilityMolecular docking and dynamicIn-silico study |
| spellingShingle | Md. Reyad-ul-Ferdous Mohnad Abdalla Yongfeng Song Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study Journal of Saudi Chemical Society Obesity Mitochondrial ATP production Mitochondrial DNA quantification Cell viability Molecular docking and dynamic In-silico study |
| title | Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study |
| title_full | Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study |
| title_fullStr | Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study |
| title_full_unstemmed | Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study |
| title_short | Glycyrrhizin (Glycyrrhizic Acid) HMGB1 (high mobility group box 1) inhibitor upregulate mitochondrial function in adipocyte, cell viability and in-silico study |
| title_sort | glycyrrhizin glycyrrhizic acid hmgb1 high mobility group box 1 inhibitor upregulate mitochondrial function in adipocyte cell viability and in silico study |
| topic | Obesity Mitochondrial ATP production Mitochondrial DNA quantification Cell viability Molecular docking and dynamic In-silico study |
| url | http://www.sciencedirect.com/science/article/pii/S1319610322000369 |
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