Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α
Ulcerative colitis (UC) is a complex inflammatory bowel disease (IBD) associated with mitochondrial function. Atractylenolide III (AT III) is a natural product with anti-inflammatory effects. The aim of this work is to investigate the protective effect of AT III on UC and its underlying mechanisms....
Saved in:
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2022/9129984 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832558600149532672 |
|---|---|
| author | Jieru Han Wenhao Li Guangyu Shi Yunlei Huang Xutao Sun Na Sun Deyou Jiang |
| author_facet | Jieru Han Wenhao Li Guangyu Shi Yunlei Huang Xutao Sun Na Sun Deyou Jiang |
| author_sort | Jieru Han |
| collection | DOAJ |
| description | Ulcerative colitis (UC) is a complex inflammatory bowel disease (IBD) associated with mitochondrial function. Atractylenolide III (AT III) is a natural product with anti-inflammatory effects. The aim of this work is to investigate the protective effect of AT III on UC and its underlying mechanisms. Herein, dextran sulfate sodium- (DSS-) induced mice and lipopolysaccharide- (LPS-) stimulated intestinal epithelial cells (IEC-6) were employed to mimic UC pathologies in vivo and in vitro. The results showed that in DSS-induced mice, AT III significantly reversed the body weight loss, colon length reduction, disease activity index (DAI) increase, and histological damage. The production of proinflammatory factors and reduction of antioxidants in colitis were suppressed by AT III. In addition, we demonstrated that AT III attenuated the intestinal epithelial barrier destruction and mitochondrial dysfunction induced by DSS, which was similar to the in vitro results in LPS-treated IEC-6 cells. The protein levels of p-AMPK, SIRT1, and PGC-1α along with acetylated PGC-1α were also upregulated by AT III in vivo and in vitro. In conclusion, these findings support that AT III may protect against mitochondrial dysfunction by the activation of the AMPK/SIRT1/PGC-1α signaling pathway during UC development. |
| format | Article |
| id | doaj-art-7698565ab80440488c0de273fb50a3fa |
| institution | Kabale University |
| issn | 1466-1861 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-7698565ab80440488c0de273fb50a3fa2025-02-03T01:32:01ZengWileyMediators of Inflammation1466-18612022-01-01202210.1155/2022/9129984Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1αJieru Han0Wenhao Li1Guangyu Shi2Yunlei Huang3Xutao Sun4Na Sun5Deyou Jiang6Department of Synopsis of the Golden ChamberDepartment of Synopsis of the Golden ChamberDepartment of Ultrasound MedicineFoundamental Training BaseDepartment of TyphoidSchool of Basic Medical SciencesDepartment of Synopsis of the Golden ChamberUlcerative colitis (UC) is a complex inflammatory bowel disease (IBD) associated with mitochondrial function. Atractylenolide III (AT III) is a natural product with anti-inflammatory effects. The aim of this work is to investigate the protective effect of AT III on UC and its underlying mechanisms. Herein, dextran sulfate sodium- (DSS-) induced mice and lipopolysaccharide- (LPS-) stimulated intestinal epithelial cells (IEC-6) were employed to mimic UC pathologies in vivo and in vitro. The results showed that in DSS-induced mice, AT III significantly reversed the body weight loss, colon length reduction, disease activity index (DAI) increase, and histological damage. The production of proinflammatory factors and reduction of antioxidants in colitis were suppressed by AT III. In addition, we demonstrated that AT III attenuated the intestinal epithelial barrier destruction and mitochondrial dysfunction induced by DSS, which was similar to the in vitro results in LPS-treated IEC-6 cells. The protein levels of p-AMPK, SIRT1, and PGC-1α along with acetylated PGC-1α were also upregulated by AT III in vivo and in vitro. In conclusion, these findings support that AT III may protect against mitochondrial dysfunction by the activation of the AMPK/SIRT1/PGC-1α signaling pathway during UC development.http://dx.doi.org/10.1155/2022/9129984 |
| spellingShingle | Jieru Han Wenhao Li Guangyu Shi Yunlei Huang Xutao Sun Na Sun Deyou Jiang Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α Mediators of Inflammation |
| title | Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α |
| title_full | Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α |
| title_fullStr | Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α |
| title_full_unstemmed | Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α |
| title_short | Atractylenolide III Improves Mitochondrial Function and Protects Against Ulcerative Colitis by Activating AMPK/SIRT1/PGC-1α |
| title_sort | atractylenolide iii improves mitochondrial function and protects against ulcerative colitis by activating ampk sirt1 pgc 1α |
| url | http://dx.doi.org/10.1155/2022/9129984 |
| work_keys_str_mv | AT jieruhan atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT wenhaoli atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT guangyushi atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT yunleihuang atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT xutaosun atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT nasun atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a AT deyoujiang atractylenolideiiiimprovesmitochondrialfunctionandprotectsagainstulcerativecolitisbyactivatingampksirt1pgc1a |