Attenuation of Hyperoxic Lung Injury by the CYP1A Inducer β–Naphthoflavone

Sinha, Anuj; Muthiah, Kathirvel; Jiang, Weiwu; Couroucli, Xanthi I.; Barrios, Roberto; Moorthy, Bhagavatula

doi:10.1093/toxsci/kfi226

Cited by 36 publications

(49 citation statements)

References 31 publications

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“…Lung microsomes were prepared by differential centrifugation, as reported previously (17), from individual animals. Protein concentrations and EROD (CYP1A1) activities in lung were assayed as we have described previously (17,19,20).…”

Section: Methodsmentioning

confidence: 99%

“…Lung microsomes (20 g of protein) prepared from individual animals were subjected to Western blotting, as described previously (17,19,20). The proteins bands on the blots were detected by chemiluminescence after exposure to x-ray films (ECL plus detection, Amersham Pharmacia Biotech, Inc., Piscataway, NJ).…”

Section: Methodsmentioning

confidence: 99%

“…The proteins bands on the blots were detected by chemiluminescence after exposure to x-ray films (ECL plus detection, Amersham Pharmacia Biotech, Inc., Piscataway, NJ). Quantitation of the blots was accomplished by densitometric scanning of the x-ray films, as described previously (19,20).…”

Section: Methodsmentioning

confidence: 99%

“…P450 enzymes, including CYP1A1, have also been implicated in the formation and further reactions of ROS, and may play a role in pulmonary oxygen toxicity (17)(18)(19)(20). The CYP enzymes are developmentally regulated (21).…”

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confidence: 99%

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Modulation of Pulmonary Cytochrome P4501A1 Expression by Hyperoxia and Inhaled Nitric Oxide in the Newborn Rat: Implications for Lung Injury

et al. 2006

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Inhaled nitric oxide (iNO), with supplemental oxygen, is used in the treatment of hypoxic respiratory failure of the newborn.In this study, we tested the hypothesis that exposure of newborn rats to iNO, hyperoxia, or iNO ϩ hyperoxia would modulate the expression of pulmonary cytochrome P450 (CYP)1A1 in relation to acute lung injury. Newborn Fischer 344 rats were maintained in room air, or exposed to iNO, hyperoxia (Ͼ95%), or iNO (20 or 40 ppm) ϩ hyperoxia for up to 168 h, and lung injury parameters and CYP1A1 expression were studied. Animals given iNO (40 ppm) ϩ hyperoxia were more susceptible to lung injury than those exposed to hyperoxia or iNO alone. On the other hand, animals exposed to iNO (20 ppm) ϩ hyperoxia did not elicit lung damage. Pulmonary CYP1A1 protein and mRNA expression were induced by hyperoxia, iNO (20 or 40 ppm), or iNO (20 ppm) ϩ hyperoxia for up to 168 h, compared with air-breathing controls. In animals given iNO (40 ppm) ϩ hyperoxia, pulmonary CYP1A1 was enhanced at 48 h, followed by downregulation at later time points. Immunohistochemistry experiments showed localization of CYP1A1 in the pulmonary epithelial and endothelial cells. In conclusion, because previous studies have shown beneficial effects of CYP1A1 induction in hyperoxic lung injury, our current observations showing maintenance of pulmonary CYP1A1 induction by iNO (20 ppm) ϩ hyperoxia through the 168-h period support the hypothesis that this phenomenon may contribute to the protective effects of iNO against hyperoxic injury. (Pediatr Res 59: [401][402][403][404][405][406] 2006)

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Modulation of Pulmonary Cytochrome P4501A1 Expression by Hyperoxia and Inhaled Nitric Oxide in the Newborn Rat: Implications for Lung Injury

et al. 2006

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“…Previous studies have indicated that α-Napthoflavone inhibits OS and serves potential roles is estrogen-induced breast carcinogenesis and ultraviolet-led human skin aging (27,28). β-Naphthoflavone has been demonstrated to protect mice against aristolochic acid-I-induced acute kidney injury, and to attenuate hyperoxic lung injury in premature infants primarily via mitigating OS (29,30). In the present study, α-and β-Naphthoflavone were identified to effectively antagonize the apoptosis-promoting effect of H 2 O 2 on neuronal SH-SY5Y cells.…”

Section: Discussionmentioning

confidence: 99%

α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage

Zhu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have demonstrated an association between neurological diseases and oxidative stress (OS).Naphthoflavone is a synthetic derivative of naturally occurring flavonoids that serves an important role in the treatment and prevention of OS-related diseases. The current study was designed to apply α-and β-Naphthoflavone individually and in combination to counteract the detrimental effects of OS on neurons in vitro. Neuronal SH-SY5Y cells were subjected to 20 µM H 2 O 2 , followed by exposure to 20 µM α-Naphthoflavone and/or 10 µM β-Naphthoflavone. Results indicated that α-and β-Naphthoflavone effectively antagonized the apoptosis-promoting effect of H 2 O 2 on neuronal SH-SY5Y cells, and that β-Naphthoflavone significantly (P<0.05) reversed H 2 O 2 -inhibited cell viability. Notably, co-treatment of α-and β-Naphthoflavone reversed the H 2 O 2 -induced apoptosis rate elevation and cell viability reduction. Further analysis demonstrated that H 2 O 2 inhibited the activities of antioxidant enzymes including catalase, superoxide dismutase and glutathione peroxidase, but this was reversed by the co-treatment with α-and β-Naphthoflavone and selectively enhanced by the treatment with α-or β-Naphthoflavone. H 2 O 2 -stimulated p38 mitogen-activated protein kinase activation was repressed following treatment with α-and/or β-Naphthoflavone, along with a decreased expression of the apoptosis-related factors and inhibited caspase-3 activation. In conclusion, co-treatment with α-and β-Naphthoflavone minimized H 2 O 2 -led neuron damage compared with treatment with α-or β-Naphthoflavone, suggesting a synergetic effect between α-and β-Naphthoflavone. This indicates that utilizing α-and β-Naphthoflavone together in the clinical setting may provide a novel therapeutic for neurological disease.

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Augmented oxygen-mediated transcriptional activation of cytochrome P450 (CYP)1A expression and increased susceptibilities to hyperoxic lung injury in transgenic mice carrying the human CYP1A1 or mouse 1A2 promoter in vivo

Jiang

Couroucli

Wang

et al. 2011

Biochemical and Biophysical Research Communications

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Supplemental oxygen administration is frequently administered to preterm and term infants having pulmonary insufficiency. However, hyperoxia contributes to the development of bronchopulmonary dysplasia (BPD) in premature infants. Cytochrome P450 (CYP)A enzymes have been implicated in hyperoxic lung injury. In this study, we tested the hypothesis that hyperoxia induces CYP1A1 and 1A2 enzymes by transcriptional activation of the corresponding promoters in vivo, and transgenic mice expressing the human CYP1A1 or the mouse 1A2 promoter would be more susceptible to hyperoxic lung injury than wild type (WT) mice. Adult WT (CD-1) (12 week-old) mice, transgenic mice carrying a 10 kb human CYP1A1 promoter and the luciferase (luc) reporter gene (CYP1A1-luc), or mice expressing the mouse CYP1A2 promoter (CYP1A2-luc) were maintained in room air or exposed to hyperoxia for 24–72 h. Hyperoxia exposure of CYP1A1-luc mice for 24 and 48 h resulted in 2.5- and 1.25-fold increases, respectively in signal intensities, compared to room air controls. By 72 h, the induction had declined to control levels. CYP1A2-luc mice also showed enhanced luc expression after 24–48 h, albeit to a lesser extent than those expressing the CYP1A1 promoter. Also, these mice showed decreased levels of endogenous CYP1A1 and 1A2 expression after prolonged hyperoxia, and were also more susceptible to lung injury than similarly exposed WT mice, with CYP1A2-luc mice showing the greatest injury. Our results support the hypothesis that hyperoxia induces CYP1A enzymes by transcriptional activation of its corresponding promoters, and that decreased endogenous expression of these enzymes contribute to the increased susceptibilities to hyperoxic lung injury in the transgenic animals. In summary, this is the first report providing direct evidence of hyperoxia-mediated induction of CYP1A1 and CYP1A2 expression in vivo by mechanisms entailing transcriptional activation of the corresponding promoters, a phenomenon that has implications for hyperoxic lung injury, as well as other pathologies caused by oxidative stress.

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Attenuation of Hyperoxic Lung Injury by the CYP1A Inducer β–Naphthoflavone

Cited by 36 publications

References 31 publications

Modulation of Pulmonary Cytochrome P4501A1 Expression by Hyperoxia and Inhaled Nitric Oxide in the Newborn Rat: Implications for Lung Injury

Modulation of Pulmonary Cytochrome P4501A1 Expression by Hyperoxia and Inhaled Nitric Oxide in the Newborn Rat: Implications for Lung Injury

α- and β-Naphthoflavone synergistically attenuate H2O2-induced neuron SH-SY5Y cell damage

Augmented oxygen-mediated transcriptional activation of cytochrome P450 (CYP)1A expression and increased susceptibilities to hyperoxic lung injury in transgenic mice carrying the human CYP1A1 or mouse 1A2 promoter in vivo

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