Liver Injury During Treatment With Rifampicin, Vancomycin, and Acetaminophen

Khanal, Subrat; Ghimire, Pranita; Dhamoon, Amit S.

doi:10.1097/mjt.0000000000000749

Cited by 3 publications

(4 citation statements)

References 10 publications

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“…CYP1A2 and CYP2E1 are two key enzymes that are evaluated due to the administration of INH and RIF. 4,5 Interestingly, we observed Dendrobine (100 and 200 mg/kg) significantly increased the levels of CYP1A2. These results supported that Dendrobine affected oxidative stress biomarkers in the liver by the regulation of CYP1A2.…”

Section: Discussionmentioning

confidence: 73%

“…4,6 However, their uses cause hepatotoxicity including liver injury and liver failure in some patients. 5 INH is metabolized into hydrazine by CYP450, which induces liver steatosis. When INH is combined with RIF, RIF is converted into desacetyl RIF by CYP450 and thereby promoting hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…When INH is combined with RIF, RIF is converted into desacetyl RIF by CYP450 and thereby promoting hepatotoxicity. 3,5 Thus, it is important to discover drug candidates to reverse liver toxicities induced by INH and/or RIF.…”

Section: Discussionmentioning

confidence: 99%

“…One of the side effects caused by the idiosyncratic metabolic products of RIF is liver injury. 5 Moreover, when RIF is combined with other antituberculosis drugs such as INH in the treatment of tuberculosis, they are more likely to cause severe liver injury for patients. 3 It is known that both INH and RIF are first-line medications used in the treatment of tuberculosis.…”

Section: Introductionmentioning

confidence: 99%

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Dendrobine attenuates isoniazid- and rifampicin-induced liver injury by inhibiting miR-295-5p

Zhang

Zhu

et al. 2020

Hum Exp Toxicol

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The present study aims to investigate the protective effects of Dendrobine and its underlying mechanisms on liver injury induced by isoniazid (INH) and rifampicin (RIF). A mouse model of liver injury was induced by intragastrically administration of 100 mg/kg INH and 100 mg/kg RIF for 14 days. The mice were intragastrically administrated with Dendrobine (50, 100, and 200 mg/kg) before the administration of INH and RIF. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. Oxidative stress markers including glutathione, superoxide dismutase, and malondialdehyde in the liver were measured and liver histopathological examinations were performed. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were applied to determine the mRNA and protein expressions, respectively. Luciferase reporter assay was used to evaluate the interactions between miR-295-5p and CYP1A2. Dendrobine significantly decreased serum ALT and AST and inhibited the liver index and ameliorated the liver histological changes induced by INH and RIF. Besides, Dendrobine also regulated oxidative stress status in the liver by the regulation of CYP1A2. Moreover, mmu-miR-295-5p was identified to target CYP1A2 and to regulate the expression of CYP1A2. In summary, Dendrobine ameliorated INH and RIF induced mouse liver injury by miR-295-5p-mediated CYP1A2 expression.

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Section: Discussionmentioning

confidence: 73%