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Emodin induces liver injury by inhibiting the key enzymes of FADH/NADPH transport in rat liver

Abstract

Emodin is a natural anthraquinone derivative that occurs in many Chinese medicinal herbs. It might induce liver damage, but the mechanism is not clear. In this research, seven groups of Sprague-Dawley (SD) rats with three doses of emodin were used. The liver injury was examined by biochemistry indexes and histopathology. Altered proteins between the control group (CG) and the liver injury group were determined by proteomic technology. The results showed that emodin had risk of liver injury and had a time- and dose-dependent. In the high-dosage 1-week group (HG1), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was down regulated, and the activity of malate dehydrogenase (MDH) was inhibited by emodin. These might cause the breakdown of FADH or NADH/NADPH transport from cytoplasm to mitochondria. The WB results showed that the inhibition of FADH/NADPH transport induced the high activity of caspase-9 and caspase-3, and the expressions of cytochrome c (Cyt C), caspase-9 and caspase-3 were high in HG1, which might lead to mitochondrial apoptosis pathway activation. Addition, whatever HG1 or low-dose group (LG), the effects of emodin on mitochondria was present. Overall, for the first time, we showed that emodin inhibited proton transport and induced the activation of the mitochondrial apoptosis pathway, which might be the reason for the liver injury.

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Publication details

The article was received on 15 Nov 2017, accepted on 09 May 2018 and first published on 14 May 2018


Article type: Paper
DOI: 10.1039/C7TX00307B
Citation: Toxicol. Res., 2018, Accepted Manuscript
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    Emodin induces liver injury by inhibiting the key enzymes of FADH/NADPH transport in rat liver

    X. Yang, Y. Zhang, Y. Liu, C. Chen, W. Xu and H. Xiao, Toxicol. Res., 2018, Accepted Manuscript , DOI: 10.1039/C7TX00307B

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