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Abstract
Oxidative stress is an important pathological mechanism in various liver diseases. Polygonum multiflorum Thunb. (PM) can be used for the treatment of diseases associated with aging, hyperlipidemia, and oxidative stress in traditional Chinese medicine. In this study, we examined the hepatoprotective effects of the ethanolic extract of PM (PME) in in vitro and in vivo models. The PME induced expression of antioxidant-response-element- (ARE-) related genes in HepG2 cells showed a dose-dependent manner. Pretreatment of HepG2 cell with PME suppressed H2O2- and acetaminophen- (APAP-) induced cellular reactive oxygen species (ROS) generation and cytotoxicity. In APAP-induced mouse liver injury, pretreatment with PME also showed ability to increase the survival rate and reduce the severity of liver injury. Treatment with PME attenuated bile duct ligation-induced extrahepatic cholestatic liver injury and further increased multidrug resistance protein 4 (MRP4) and reduced organic anion-transporting polypeptide (OATP) expression. Furthermore, increased nuclear translocation of the nuclear factor erythroid 2-related factor 2 (Nrf2) was observed after treatment with PME in both in vivo models. In conclusion, the current study showed the hepatoprotective activity of PME by regulating the redox state in liver injury through Nrf2 activation and controlling hepatic bile acid homeostasis in obstructive cholestasis, through bile acid transporter expression modulation.
Highlights
Oxidative stress is widely recognized as a detrimental pathological mechanism for the initiation and progression of various liver diseases
PM extracted with 50% ethanol (PME) treatment for 6 h upregulated the mRNA expression of genes downstream of nuclear factor erythroid 2-related factor 2 (Nrf2), including heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase (NQO1), and the glutamate–cysteine ligase catalytic subunit (GCLc), in a dose-dependent manner (Figures 1(b)–1(d))
We further examined the protective effects of PME against Reactive oxygen species (ROS) production in HepG2 cells
Summary
Oxidative stress is widely recognized as a detrimental pathological mechanism for the initiation and progression of various liver diseases. Reactive oxygen species (ROS) are mainly generated by cytochrome P450 enzymes in the mitochondria of hepatocytes. When excess ROS are generated, they interact with proteins, DNA, and lipids, resulting in cell injury. In the course of liver diseases, either from inflammatory or metabolic insults, disruption of the balance between oxidant and antioxidant mechanisms is commonly observed [1, 2]. The abilities of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), to increase the expressions of antioxidant proteins and suppress oxidative stress-related injury have been extensively studied [3, 4]. Nrf2activating regimens may be used for liver diseases
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