Abstract
Herba Epimedii, a commonly used Chinese medicine, has attracted much attention recently because of its potential hepatotoxic effects. 2″-O-Rhamnosyl icariside II, baohuoside I and baohuoside II are the main components of Herba Epimedii, and previous research indicates that these three compounds are related to the hepatotoxicity of Herba Epimedii. To test this idea, in this study, HL-7702 and HepG2 cells were chosen as the in vitro models and the influences of these three compounds on a series of cytotoxicity indices, including ALT, AST, LDH, SOD, GSH, MDA, ROS and MMP, were determined. The results showed that at certain concentrations, the three compounds had different effects on the indices. Among them, baohuoside I at high concentration (32 μg/mL) displayed more significant cytotoxicity than the other two compounds; therefore, it was inferred to be more closely correlated with the liver injury induced by Herba Epimedii combined with the previous study, and its toxic mechanisms may be involved in increasing oxidative stress and inducing apoptosis. The findings of this study may provide evidence of the toxic composition of Herba Epimedii to preliminarily discuss the toxic mechanisms and provide improved guidance for its clinical safety.
Highlights
Drug-induced liver injury (DILI) is an unresolved clinical problem and is the most frequent cause of post-marketing withdrawal of new medications [1]
The ALT, AST and lactate dehydrogenase (LDH) activity measurement results are shown in Figure 2, where the three drugs did not lead to an increased release of ALT in HL-7702 (Figure 2a–c) and HepG2 (Figure 2d–f) cells. 200 -O-Rhamnosyl icariside II at measurement results are shown in Figure 2, where the three drugs did not lead to an increased release in HL-7702 (Figure 2a–c) and HepG2 (Figure 2d–f) cells. 2′′-O-Rhamnosyl icariside
This article aimed to evaluate the influence of hepatotoxic suspicions of Herba Epimedii, 200 -O-rhamnosyl icariside II, baohuoside I and baohuoside II on liver cells in vitro
Summary
Drug-induced liver injury (DILI) is an unresolved clinical problem and is the most frequent cause of post-marketing withdrawal of new medications [1]. DILI can affect both parenchymal and nonparenchymal cells of the liver, leading to a wide variety of pathological changes, mainly including acute and chronic hepatocellular steatosis, fibrosis, cirrhosis, cholestasis and hepatitis [3,4]. The predominant clinical manifestations of DILI are acute hepatitis, cholestasis, and a mixed pattern [5]. There are still serious limitations in current knowledge regarding the clinical diagnosis of DILI and the hepatotoxic prediction of drugs due to various confounding factors. Many potential hepatotoxic drugs fail to be identified in time during clinical trials or application, and their DILI has been ignored or underestimated and has damaged public health and drug development. To better evaluate a drug’s potential hepatotoxicity and more effectively reduce the occurrence of DILI, it is imperative to analyze the reasons and explore the mechanisms of DILI
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