Cytoprotective Effect of Ligustrum robustum Polyphenol Extract against Hydrogen Peroxide-Induced Oxidative Stress via Nrf2 Signaling Pathway in Caco-2 Cells.

Jiayi Chen,Tao Zhou,Fangting He,Chunping Jiang,Saira Baloch,Sijing Liu,Xiaofang Pei

doi:10.1155/2019/5026458

Jiayi Chen, Tao Zhou + Show 5 more

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https://doi.org/10.1155/2019/5026458

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Abstract

Ligustrum robustum is a traditional herbal tea that is widely distributed in southwest China. The health effects of L. robustum are characteristics of clearing heat, antioxidant, inducing resurgence, and improving digestion. However, the molecular mechanisms related to these effects, particularly the antioxidant mechanism, have been seldom reported. The objective of this study was to assess antioxidative capacity of L. robustum, and its protective effects and mechanisms against hydrogen peroxide (H2O2) - induced toxicity in Caco-2 cells. Total phenolic contents, free radical scavenging activity, and reducing capacity of L. robustum were measured. The effects of L. robustum on the cell viability and antioxidant defense system were explored. The expression of nuclear factor E2 related factor 2 (Nrf2) and antioxidant genes: quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), and glutamate cysteine ligase (GCL) were analyzed by western blot and qPCR. Pretreatment of L. robustum could significantly reduce H2O2-induced toxicity, decrease the level of reactive oxygen species (ROS) and malondialdehyde (MDA), and increase the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR). By activating the expression of Nrf2 and antioxidant genes (NQO1, HO-1, and GCL), L. robustum exerts cytoprotective effect in Caco-2 cells dealt with H2O2. Therefore, the well-established model of Caco-2 cells demonstrates that L. robustum may modulate the cytoprotective effect against the H2O2-induced oxidative stress through the Nrf2 signaling pathway.

Highlights

Oxidative stress (OS) refers to the disequilibrium in the production and degradation of reactive oxygen species (ROS)
When exposed to H2O2, the viability of Caco2 cells, which was only 36.2%, decreased compared to control cells, whereas the pretreated with butanol extracts (BuE) (162.5mg/l, 81.3mg/l, and 40.6mg/l), cell viability increased by 75.3%, 47.8%, and 31.2% in comparison to the model group (Figure 1)
BuE significantly abrogated H2O2-induced cytotoxicity in a dosedependent manner. These findings demonstrated that BuE of L. robustum has significant cytoprotective effects on H2O2induced cytotoxicity in Caco-2 cells

Summary

Introduction

Oxidative stress (OS) refers to the disequilibrium in the production and degradation of reactive oxygen species (ROS). Excessive production of ROS may damage biomolecules and lead to the pathological changes, such as inflammation, cancer, neurodegeneration, cardiovascular diseases, and inflammatory bowel disease (IBD) [2, 3]. Activation of antioxidant defense systems could benefit cells survival [4, 5]. Nrf will activate, translocate into the nucleus, and bind to antioxidant response element (ARE) [6]. Nrf2-ARE initiates cellular defense by induction of phase II detoxifying and antioxidant enzymes, i.e., quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), and catalase (CAT) [6]

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