Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways
<i>Angelicae pubescentis</i> radix (APR) has been traditionally used for thousands of years in China to treat rheumatoid arthritis (RA), an autoimmune disorder. As the main active coumarin of APR, columbianadin (CBN) exhibits a significant anti-inflammatory effect in vitro. However, the...
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MDPI AG
2024-03-01
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author | Zhe Ma Lin Peng Yaoyao Sheng Wenhui Chu Yongqian Fu |
author_facet | Zhe Ma Lin Peng Yaoyao Sheng Wenhui Chu Yongqian Fu |
author_sort | Zhe Ma |
collection | DOAJ |
description | <i>Angelicae pubescentis</i> radix (APR) has been traditionally used for thousands of years in China to treat rheumatoid arthritis (RA), an autoimmune disorder. As the main active coumarin of APR, columbianadin (CBN) exhibits a significant anti-inflammatory effect in vitro. However, the anti-inflammatory activity and underlying mechanism of CBN in vivo remain unclear. This work aimed to elucidate the anti-inflammatory activity of CBN in vivo and its related signaling pathways in a D-Gal-induced liver injury mouse model. Analysis of biochemical indices (ALT and AST) and pro-inflammatory cytokines (IL-1β and IL-6) in serum indicated that CBN significantly ameliorated D-Gal-induced liver injury. CBN treatment also significantly increased the activities of antioxidant enzymes (SOD, CAT, GPx), and decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in liver tissue. Liver histology revealed that CBN treatment reduced hepatic inflammation. Western blot analysis indicated that CBN down-regulates the expression of phosphorylated JAK2, STAT3, MAPK, and NF-κB in the related signaling pathways. These findings support the traditional use of APR as a remedy for the immune system, and indicate that the JAK2/STAT3 and JAK2/p38/NF-κB signaling pathways may be important mechanisms for the anti-inflammatory activity of CBN in vivo. |
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spelling | doaj.art-bb354c7684d74df0b13f71cba68274382024-03-27T13:59:26ZengMDPI AGPharmaceuticals1424-82472024-03-0117337810.3390/ph17030378Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB PathwaysZhe Ma0Lin Peng1Yaoyao Sheng2Wenhui Chu3Yongqian Fu4School of Life Science, Taizhou University, 1139 Shifu Avenue, Taizhou 318000, ChinaSchool of Life Science, Taizhou University, 1139 Shifu Avenue, Taizhou 318000, ChinaSchool of Life Science, Taizhou University, 1139 Shifu Avenue, Taizhou 318000, ChinaSchool of Life Science, Taizhou University, 1139 Shifu Avenue, Taizhou 318000, ChinaSchool of Life Science, Taizhou University, 1139 Shifu Avenue, Taizhou 318000, China<i>Angelicae pubescentis</i> radix (APR) has been traditionally used for thousands of years in China to treat rheumatoid arthritis (RA), an autoimmune disorder. As the main active coumarin of APR, columbianadin (CBN) exhibits a significant anti-inflammatory effect in vitro. However, the anti-inflammatory activity and underlying mechanism of CBN in vivo remain unclear. This work aimed to elucidate the anti-inflammatory activity of CBN in vivo and its related signaling pathways in a D-Gal-induced liver injury mouse model. Analysis of biochemical indices (ALT and AST) and pro-inflammatory cytokines (IL-1β and IL-6) in serum indicated that CBN significantly ameliorated D-Gal-induced liver injury. CBN treatment also significantly increased the activities of antioxidant enzymes (SOD, CAT, GPx), and decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in liver tissue. Liver histology revealed that CBN treatment reduced hepatic inflammation. Western blot analysis indicated that CBN down-regulates the expression of phosphorylated JAK2, STAT3, MAPK, and NF-κB in the related signaling pathways. These findings support the traditional use of APR as a remedy for the immune system, and indicate that the JAK2/STAT3 and JAK2/p38/NF-κB signaling pathways may be important mechanisms for the anti-inflammatory activity of CBN in vivo.https://www.mdpi.com/1424-8247/17/3/378anti-inflammationcolumbianadincoumarinsD-galactose-induced liver injuryoxidative stress |
spellingShingle | Zhe Ma Lin Peng Yaoyao Sheng Wenhui Chu Yongqian Fu Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways Pharmaceuticals anti-inflammation columbianadin coumarins D-galactose-induced liver injury oxidative stress |
title | Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways |
title_full | Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways |
title_fullStr | Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways |
title_full_unstemmed | Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways |
title_short | Anti-Inflammatory Effect of Columbianadin against D-Galactose-Induced Liver Injury In Vivo via the JAK2/STAT3 and JAK2/p38/NF-κB Pathways |
title_sort | anti inflammatory effect of columbianadin against d galactose induced liver injury in vivo via the jak2 stat3 and jak2 p38 nf κb pathways |
topic | anti-inflammation columbianadin coumarins D-galactose-induced liver injury oxidative stress |
url | https://www.mdpi.com/1424-8247/17/3/378 |
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