Radiosynovectomy of small and medium joints

Liepe, Knut

doi:10.1016/b978-0-12-822960-6.00025-9

Cited by 1 publication

(1 citation statement)

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“…Triptolide is mainly used for the treatment of autoimmune diseases and inflammatory diseases including rheumatoid arthritis ( Fan et al, 2018 ), ankylosing spondylitis ( Guo et al, 1981 ), and lupus erythematosus ( Liu Y. F et al, 2019 ; Xiao et al, 2022 ). The inflammatory state of these patients ( Ferrara et al, 2011 ; Kuhn et al, 2021 ; Liepe, 2021 ) may increase the sensitivity of the body to drug-induced toxicity ( Darehgazani et al, 2016 ; Kubes and Jenne, 2018 ). However, current studies of triptolide-induced hepatotoxicity were mainly conducted with experimental animals in a healthy state ( Lu et al, 2017 ; Miao et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Inflammation aggravated the hepatotoxicity of triptolide by oxidative stress, lipid metabolism disorder, autophagy, and apoptosis in zebrafish

Zhang

Zhu

et al. 2022

Front. Pharmacol.

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Triptolide is a major compound isolated from the Tripterygium wilfordii Hook that is mainly used for the treatment of autoimmune disorders and inflammatory diseases. Though triptolide-induced hepatotoxicity has been widely reported, the hepatic effects when the patients are in an inflammatory state are not clear. In this study, we used low-dose Lipopolysaccharides (LPS) to disrupt the inflammation homeostasis in the liver of zebrafish and explored the hepatotoxicity of triptolide under an inflammatory state. Compared with the Triptolide group, LPS-Triptolide cotreatment exacerbate the liver injury with a remarkable decrease of liver size and liver-specific fluorescence intensity, accompanied by significant elevation of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Liver cell damages were further demonstrated by histological staining and scanning electron microscopy observation. Lipid metabolism was severely impaired as indicated by delayed yolk sac absorption, accumulated triglycerides in the liver, and dysregulation of the related genes, such as ppar-α, cpt-1, mgst, srebf1/2, and fasn. Oxidative stress could be involved in the molecular mechanism as the Nrf2/keap1 antioxidant pathways were down-regulated when the zebrafish in an inflammatory state. Moreover, the expression of autophagy-related genes such as beclin, atg5, map1lc3b, and atg3 was also dysregulated. Finally, apoptosis was significantly induced in responses to LPS-Triptolide co-treatment. We speculate that triptolide could exacerbate the immune response and impair lipid metabolism, resulting in enhanced sensitivity of the zebrafish liver to triptolide-induced toxic effects through disruption of the antioxidant system and induction of apoptosis.

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