Luteoloside Acts as 3C Protease Inhibitor of Enterovirus 71 In Vitro

Cao, Zhipeng; Ding, Yue; Ke, Zhipeng; Cao, Liang; Li, Na; Ding, Gang; Wang, Zhenzhong; Xiao, Wei

doi:10.1371/journal.pone.0148693

Cited by 40 publications

(28 citation statements)

References 49 publications

(63 reference statements)

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“…Many studies have shown that flavonoids may protect cardiomyocytes against I/R injury (Yuan et al, ; Zhang et al, ). Lut, a flavonoid compound extracted from honeysuckle, exhibits anti‐inflammatory, antiviral, and anticancer properties (Cao et al, ; Hwang, Lee, Kim, & Hwang, ; Jung, Jin, Min, Kim, & Choi, ; Tian et al, ) and has shown promising results in myocardial cells. A/R injury was used to model I/R injury in vitro.…”

Section: Discussionmentioning

confidence: 99%

Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein

Liu

Yang²,

Huang

et al. 2018

Phytotherapy Research

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Ischemia/reperfusion (I/R) injury is the major cause of acute cardiovascular disease worldwide. 14-3-3η protein has been demonstrated to protect myocardium against I/R injury. Luteoloside (Lut), a flavonoid found in many Chinese herbs, exerts myocardial protection effects. However, the mechanism remains unclear. We hypothesize that the cardioprotective role of Lut is exerted by regulating the 14-3-3η signal pathway. To investigate our hypothesis, an in vitro I/R model was generated in H9C2 cardiomyocytes by anoxia/reoxygenation (A/R) treatment. The effects of Lut on cardiomyocytes with A/R injury were assessed by determining the cell viability, lactate dehydrogenase levels, intracellular reactive oxygen species levels, mitochondrial permeability transition pores (mPTP) openness, caspase-3 activity, and apoptosis rate. The effects on protein expression were tested using western blot analysis. Lut attenuated A/R-induced injury to cardiomyocytes by increasing the expression of 14-3-3η protein and cell viability; decreasing levels of lactate dehydrogenase, reactive oxygen species, mPTP openness, caspase-3 activity, and low apoptosis rate were observed. However, the cardioprotective effects of Lut were blocked by AD14-3-3ηRNAi, an adenovirus knocking down the intracellular 14-3-3η expression. In conclusion, to our knowledge, this is the first study to demonstrate that Lut protected cardiomyocytes from A/R-induced injury via the regulation of 14-3-3η signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein

Liu

Yang²,

Huang

et al. 2018

Phytotherapy Research

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“…This analysis was performed as previously described 9 , 66 , 67 . Briefly, Vero cells (1 × 10 6 cells/well) seeded into 6-well plates were infected with EV71 (100 TCID 50 ) at 37 °C for 2 h. After removing the virus, the infected cells were treated with 100 µM ICAC.…”

Section: Methodsmentioning

confidence: 99%

Isochlorogenic acid C prevents enterovirus 71 infection via modulating redox homeostasis of glutathione

Cao

Ding

Cao

et al. 2017

Sci Rep

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Enterovirus 71 (EV71) is a key pathogen of hand, foot and mouth disease (HFMD) in children under 6 years of age. The antiviral potency of antioxidant isochlorogenic acid C (ICAC) extracted from foods was evaluated in cellular and animal models. First, the cytotoxicity of ICAC on Vero cells was investigated. The viral plaques, cytopathic effects and yield induced by EV71 infection were obviously reduced by ICAC, which was consistent with the investigation of VP1 transcripts and protein expression. Moreover, the mortality, weight loss and limb paralysis of mice caused by EV71 challenge were remarkably relieved by ICAC injection, which was achieved through decreases in the viral load and cytokine secretion in the mouse brain. Further biochemical assays showed that ICAC modulated several antioxidant enzymes involved in reduced and oxidized glutathione (GSH and GSSG) homeostasis, including glutathione reductase (GR), glutathione peroxidase (GPX), and glucose-6-phosphate dehydrogenase (G6PD), resulting in restoration of the GSH/GSSG ratio and reactive oxygen species (ROS) level. Finally, the antiviral effects of ICAC were dose-dependently disrupted by BSO, a biosynthesis inhibitor of GSH. This study indicated that ICAC acted as an antioxidant and prevented EV71 infection by modulating the redox homeostasis of glutathione.

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“…5 Luteolin has considerable pharmacological value, including antitumor, antioxidative, neuroprotective, and anti-inflammatory effects. [6][7][8][9] The anticancer effect of luteolin has been investigated in various cancers. [10][11][12][13][14][15] For example, luteolin inhibited the proliferation of human cholangiocarcinoma cells by inducing apoptosis and interrupting OncoTargets and Therapy 2019:12 submit your manuscript | www.dovepress.com…”

Section: Introductionmentioning

confidence: 99%

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

You¹,

Wang²,

Shao

et al. 2019

OTT

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Purpose Glioma is a malignant tumor that originates in the brain and spine and is difficult to be completely removed. Though glioma patients receive active treatment, the survival rate is still poor. Therefore, it is urgent to discover a new medicine to treat glioma patients in order to improve the survival rate. In this study, we explored the anticancer effect and the potential mechanism of luteolin on glioma in vitro. Materials and methods Cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Fluorescent microscopy and flow cytometry analysis were used to determine the cellular apoptosis. Western blot analysis was performed to explore the changes in protein expression. Quantitative reverse transcription-PCR (qRT-PCR) analysis was utilized to evaluate the expression level of the tumor suppressor miR-124-3p. Results CCK-8 assays indicated that luteolin significantly inhibited glioma cell proliferation in a time- and dose-dependent manner. Fluorescent microscopy and flow cytometry analysis confirmed that luteolin induced glioma cell apoptosis. Western blot analysis showed that luteolin induced cellular apoptosis in glioma cells via MAPK activation (JNK, ERK, and p38). Luteolin stimulated the death receptor (FADD) to regulate the apoptosis proteins (Caspase-8, Caspase-3, and PARP). Luteolin increased the expression levels of LC3B II/I and downregulated the level of p62 that promotes cell autophagy. Finally, qRT-PCR confirmed that luteolin upregulated the expression levels of miR-124-3p. Conclusion These findings illustrate that luteolin may be a potential drug for glioma treatment.

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Luteoloside Acts as 3C Protease Inhibitor of Enterovirus 71 In Vitro

Cited by 40 publications

References 49 publications

Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein

Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein

Isochlorogenic acid C prevents enterovirus 71 infection via modulating redox homeostasis of glutathione

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

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