Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice
Diabetic nephropathy (DN) is a major cause of end-stage renal disease (ESRD). Glycyrrhizic acid (GA) is an effective inhibitor of reactive oxygen species (ROS) production. We investigated the role of GA in the progression of renal injury in DN. Albumin (Alb)/creatinine (crea) levels were significant...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2017/2865912 |
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| author | Shaozhang Hou Ting Zhang Yuan Li Fengying Guo Xiu Jin |
| author_facet | Shaozhang Hou Ting Zhang Yuan Li Fengying Guo Xiu Jin |
| author_sort | Shaozhang Hou |
| collection | DOAJ |
| description | Diabetic nephropathy (DN) is a major cause of end-stage renal disease (ESRD). Glycyrrhizic acid (GA) is an effective inhibitor of reactive oxygen species (ROS) production. We investigated the role of GA in the progression of renal injury in DN. Albumin (Alb)/creatinine (crea) levels were significantly lower, and renal histopathology was attenuated in the diabetic db/db mice that were treated with GA (15 mg/kg via intraperitoneal injection) once per day for eight weeks. These changes were associated with significantly lower levels of α-smooth muscle actin (α-SMA) and transforming growth factor β1 (TGF-β1) expression. Additionally, diabetic db/db mice displayed more terminal deoxynucleotidyl transferase-mediated nick-end labeling- (TUNEL-) positive nuclei and diabetes-induced ROS production in the kidneys, and these effects were attenuated by the treatment with GA, which activated adenosine monophosphate-activated protein kinase (AMPK)/silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) signaling in the kidneys. In summary, in diabetic db/db mice, the effect of GA on DN involved, in part, the inhibition of ROS and the activation of AMPK/SIRT1/PGC-1α signaling in the kidneys. GA, therefore, shows therapeutic potential for preventing and treating DN. |
| format | Article |
| id | doaj-art-e625376dbf2549bea9ac72a07783431f |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-e625376dbf2549bea9ac72a07783431f2025-08-20T03:26:04ZengWileyJournal of Diabetes Research2314-67452314-67532017-01-01201710.1155/2017/28659122865912Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db MiceShaozhang Hou0Ting Zhang1Yuan Li2Fengying Guo3Xiu Jin4Department of Pathology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, ChinaDepartment of Pathology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, ChinaDepartment of Nursing, Ningxia Medical University, Yinchuan 750004, ChinaDepartment of Pathology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, ChinaAffiliated Hospital of Jining Medical College, Jining 272000, ChinaDiabetic nephropathy (DN) is a major cause of end-stage renal disease (ESRD). Glycyrrhizic acid (GA) is an effective inhibitor of reactive oxygen species (ROS) production. We investigated the role of GA in the progression of renal injury in DN. Albumin (Alb)/creatinine (crea) levels were significantly lower, and renal histopathology was attenuated in the diabetic db/db mice that were treated with GA (15 mg/kg via intraperitoneal injection) once per day for eight weeks. These changes were associated with significantly lower levels of α-smooth muscle actin (α-SMA) and transforming growth factor β1 (TGF-β1) expression. Additionally, diabetic db/db mice displayed more terminal deoxynucleotidyl transferase-mediated nick-end labeling- (TUNEL-) positive nuclei and diabetes-induced ROS production in the kidneys, and these effects were attenuated by the treatment with GA, which activated adenosine monophosphate-activated protein kinase (AMPK)/silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) signaling in the kidneys. In summary, in diabetic db/db mice, the effect of GA on DN involved, in part, the inhibition of ROS and the activation of AMPK/SIRT1/PGC-1α signaling in the kidneys. GA, therefore, shows therapeutic potential for preventing and treating DN.http://dx.doi.org/10.1155/2017/2865912 |
| spellingShingle | Shaozhang Hou Ting Zhang Yuan Li Fengying Guo Xiu Jin Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice Journal of Diabetes Research |
| title | Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice |
| title_full | Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice |
| title_fullStr | Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice |
| title_full_unstemmed | Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice |
| title_short | Glycyrrhizic Acid Prevents Diabetic Nephropathy by Activating AMPK/SIRT1/PGC-1α Signaling in db/db Mice |
| title_sort | glycyrrhizic acid prevents diabetic nephropathy by activating ampk sirt1 pgc 1α signaling in db db mice |
| url | http://dx.doi.org/10.1155/2017/2865912 |
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