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Therapeutic potential of Shaoyao Gancao Decoction in mitigating anti‐tuberculosis drug‐induced liver injury through Nrf‐2/HO‐1/NF‐κB signaling
Tuberculosis (TB) is a persistent global health issue, evidenced by an increasing number of cases. Although anti‐TB drugs have proven efficacy, they are often associated with severe liver injury (ATB‐DILI). The objective of this research was to uncover the mechanisms through which Shaoyao Gancao Dec...
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Published in: | Biomedical chromatography 2024-12, Vol.38 (12), p.e6016-n/a |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Tuberculosis (TB) is a persistent global health issue, evidenced by an increasing number of cases. Although anti‐TB drugs have proven efficacy, they are often associated with severe liver injury (ATB‐DILI). The objective of this research was to uncover the mechanisms through which Shaoyao Gancao Decoction (SGD) mitigates ATB‐DILI, emphasizing the role of the Nrf‐2/HO‐1/NF‐κB signaling pathway. We prepared SGD granules and subjected them to HPLC‐MS/MS for analysis. An ATB‐DILI rat model was then developed and administered SGD. We evaluated liver injury markers, the extent of oxidative stress, inflammation, and the principal proteins involved in the Nrf‐2/HO‐1/NF‐κB pathway. Additionally, network pharmacology techniques were utilized to discern potential SGD targets and their associated pathways. Administering SGD had a notable effect in counteracting the elevation of liver injury markers and pathological alterations induced by ATB‐DILI. Moreover, there was a marked reduction in oxidative stress and inflammation in the treated rats. We identified 12 active compounds in SGD, with 88 shared targets between SGD and ATB‐DILI. Subsequent KEGG analysis brought attention to pathways like MAPK, NF‐κB, and IL‐17 signaling. Our findings pave the way for more in‐depth studies into the application of SGD in treating drug‐induced liver injuries. |
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ISSN: | 0269-3879 1099-0801 1099-0801 |
DOI: | 10.1002/bmc.6016 |