氧化应激
肝损伤
药理学
四氯化碳
活性氧
丙氨酸转氨酶
天冬氨酸转氨酶
谷胱甘肽
对乙酰氨基酚
抗氧化剂
化学
四氯化碳
医学
生物化学
碱性磷酸酶
内科学
酶
有机化学
作者
Xu Yifan,Jingfeng Huang,Zhuang Huichuan,Lin Junqian,Zhenzhou Jiang,Lixin Sun,Xin Huang,Luyong Zhang,Tao Wang
出处
期刊:Toxicology Research
[Oxford University Press]
日期:2024-05-01
卷期号:13 (3)
标识
DOI:10.1093/toxres/tfae073
摘要
Abstract Background Picroside II (PII), an iridoid glycoside extracted from the rhizomes and stems of the genus Picroside, exhibits pronounced hepatoprotective properties. Pre-administration of PII protects against acute liver injury caused by D-galactosamine (D-Gal), carbon tetrachloride (CCl4), and acetaminophen (APAP). This study aimed to elucidate the ramifications of PII administration subsequent to the initiation of acute hepatic injury. Methods Exploring the role of PII treatment in APAP-treated cell and rat models and in D-Gal and CCl4-treated rat models. Results In rats, APAP treatment increased serum aspartate transaminase, alanine transaminase, and alkaline phosphatase levels and decreased glutathione activity and the fluidity of the liver mitochondrial membrane. In L-02 cells, APAP exposure resulted in a decrement in membrane potential, an augmentation in the liberation of reactive oxygen species, and an acceleration of apoptotic processes. Moreover, PII pre-administration protected against D-Gal-induced acute hepatic injury and CCl4-induced chronic hepatic injury in rodent models, whereas PII administration post-injury aggravated CCl4-induced chronic hepatic injury. Conclusions Our results suggest that the effects of PII depend on the hepatic physiological or pathological state at the time of intervention. While PII possesses the potential to avert drug-induced acute hepatic injury through the mitigation of oxidative stress, its administration post-injury may exacerbate the hepatic damage, underscoring the critical importance of timing in therapeutic interventions.
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