Protection by chrysin, apigenin, and luteolin against oxidative stress is mediated by the Nrf2-dependent up-regulation of heme oxygenase 1 and glutamate cysteine ligase in rat primary hepatocytes

Huang, Chin-Shiu; Lii, Chong‐Kuei; Lin, Ai-Hsuan; Yeh, Yu‐Wen; Yao, Hsien-Tsung; Li, Chien−Chun; Wang, Tsu-Shing; Chen, Haw‐Wen

doi:10.1007/s00204-012-0913-4

Cited by 150 publications

(97 citation statements)

References 54 publications

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“…Accumulating evidence indicates that nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is involved in the protective effects of luteolin against oxidative stress (32,57–60). Furthermore, Nrf2, as the guardian of redox homeostasis, activates a battery of antioxidant and cytoprotective genes that share in common a cis -acting enhancer sequence termed antioxidant response element (ARE) that include HO-1 in response to oxidative stress (61).…”

Section: Discussionmentioning

confidence: 99%

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Xiong

Wang

Yuan

et al. 2016

International Journal of Molecular Medicine

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Reseda odorata L. has long been used in traditional Asian medicine for the treatment of diseases associated with oxidative injury and acute inflammation, such as endotoxemia, acute lung injury, acute myocardial infarction and hepatitis. Luteolin, the main component of Reseda odorata L., which is also widely found in many natural herbs and vege tables, has been shown to induce heme oxygenase-1 (HO-1) expression to exert anti-inflammatory and antioxidant effects. In this study, we aimed to examine the effects of luteolin on mice with severe acute pancreatitis (SAP), and to explore the underlying mechanisms. Cerulein and lipopolysaccharide were used to induce SAP in male Institute of Cancer Research (ICR) mice in the SAP group. The SAP group was divided into 4 subgroups, as follows: the vehicle, luteolin, zinc protoporphyrin (ZnPP) only, and luteolin (Lut) + ZnPP (luteolin plus zinc protoporphyrin treatment) groups. The wet/dry weight ratios, hematoxylin and eosin staining and pathological scores of pancreatic tissues were assessed and compared to those of the control mice. Amylase, lipase, nuclear factor-κB (NF-κB) and myeloperoxidase activities, and malondialdehyde, tumor necrosis factor α (TNFα), interleukin (IL)-6, IL-10 and HO-1 levels, as well as the expression of HO-1 were determined in serum and/or pancreatic tissue samples. SAP was successfully induced in male mice compared to normal control mice. The wet/dry weight ratios, pathological scores, and amylase and lipase activity, as well as the levels of TNFα and IL-6 were significantly reduced in the pancreatic tissues of the mice in the Lut group compared with those of the mice in the vehicle group. The Lut group exhibited a significant increase in HO-1 expression in the pancreas and enhanced serum HO-1 and IL-10 levels compared with the vehicle group. The suppression of HO-1 activity in the ZnPP group significantly abolished the protective effects of luteolin. NF-κB expression in the pancreatic tissues from the mice in the Lut + ZnPP group was significantly increased following the suppression of HO-1 activity. On the whole, our findings demonstrate that luteolin protects mice from SAP by inducing HO-1-mediated anti-inflammatory and antioxidant activities, in association with the suppression of the activation of the NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Xiong

Wang

Yuan

et al. 2016

International Journal of Molecular Medicine

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“…In cystic fibrosis bronchial cells, the expression of the pro-inflammatory IL-8 gene was suppressed by apigenin (16). In addition, apigenin has been indicated to exert a protective effect against oxidative stress (17)(18)(19). Furthermore, apigenin inhibits TGF-β1-induced collagen production and fibroblast-to-myofibroblast transition in human lung fibroblast populations (20,21).…”

Section: Discussionmentioning

confidence: 99%

Apigenin protects against bleomycin-induced lung fibrosis in rats

Chen

Zhao

2015

Experimental and Therapeutic Medicine

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Abstract. Apigenin is a non-toxic and non-mutagenic flavone that exists abundantly in numerous herbs and vegetables. Apigenin exerts anti-proliferative and anti-inflammatory properties. The aim of the present study was to investigate the effects of apigenin on bleomycin-induced lung fibrosis in rats. A single intratracheal instillation of bleomycin (5 mg/kg) was administered and rats were sacrificed on 7 and 28 days post bleomycin instillation. The instillation of bleomycin resulted in decreased body weight and an increase in the lung index. In addition, bleomycin administration increased the hydroxyproline content, myeloperoxidase (MPO) activity, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β levels and decreased the superoxide dismutase (SOD) activity in the rat lung tissues. Excessive collagen deposits were detected in the lung tissues in bleomycin-treated rats compared with normal control rats. Notably, the oral administration of apigenin (10, 15 and 20 mg/kg/day) appeared to prevent the fibrotic process. The treatment suppressed the increases in hydroxyproline content, MPO activity, TNF-α and TGF-β levels and attenuated the reduction of SOD activity that were induced by bleomycin. Furthermore, excessive collagen deposition was inhibited by the apigenin treatment. Collectively, these results suggest that apigenin may function as a potent anti-inflammatory and anti-fibrotic agent against bleomycin-induced lung fibrosis.

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“…Interestingly, also opposite activity of apigenin, luteolin and chrysin was reported. In rat primary hepatocytes and skin epidermal JB6 P+ cells these flavones induced Nrf2/ARE response and protected against oxidative stress [71, 72]. Differences in their activity between normal and cancer cells and encourage further investigation of their potential in in vivo studies and clinical trials.…”

Section: Natural Products Targeting Nrf2 Pathwaymentioning

confidence: 99%

Inhibition of cancer antioxidant defense by natural compounds

et al. 2016

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All classic, non-surgical anticancer approaches like chemotherapy, radiotherapy or photodynamic therapy kill cancer cells by inducing severe oxidative stress. Even tough chemo- and radiotherapy are still a gold standard in cancer treatment, the identification of non-toxic compounds that enhance their selectivity, would allow for lowering their doses, reduce side effects and risk of second cancers. Many natural products have the ability to sensitize cancer cells to oxidative stress induced by chemo- and radiotherapy by limiting antioxidant capacity of cancer cells. Blocking antioxidant defense in tumors decreases their ability to balance oxidative insult and results in cell death. Though one should bear in mind that the same natural compound often exerts both anti-oxidant and pro-oxidant properties, depending on concentration used, cell type, exposure time and environmental conditions. Here we present a comprehensive overview of natural products that inhibit major antioxidant defense mechanisms in cancer cells and discuss their potential in clinical application.

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Protection by chrysin, apigenin, and luteolin against oxidative stress is mediated by the Nrf2-dependent up-regulation of heme oxygenase 1 and glutamate cysteine ligase in rat primary hepatocytes

Cited by 150 publications

References 54 publications

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Luteolin protects mice from severe acute pancreatitis by exerting HO-1-mediated anti-inflammatory and antioxidant effects

Apigenin protects against bleomycin-induced lung fibrosis in rats

Inhibition of cancer antioxidant defense by natural compounds

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