Quercetin protects HCT116 cells from Dichlorvos-induced oxidative stress and apoptosis

Salem, Intidhar Ben; Boussabbeh, Manel; Graiet, Imen; Rhouma, Asma; Bacha, Hassen; Essefi, Salwa Abid

doi:10.1007/s12192-015-0651-7

Cited by 28 publications

(17 citation statements)

References 45 publications

(41 reference statements)

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“…Intestinal absorption kinetic experiments in mouse intestinal cells in vivo and human intestinal cells in vitro showed that Que had good intestinal absorption efficiency [ 26 , 27 ]. Ben et al [ 28 ] reported that Que could protect the human colon cancer cell line, HCT116, from exposure to dichlorvos, inhibiting apoptosis by regulating the redox system in HCT116. However, there is not much detailed evidence to support whether or not Que promotes the proliferation of porcine small intestinal epithelial cells, and whether or not Que has any inhibitory effect on oxidative damage in porcine intestinal epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Effects of Quercetin on Proliferation and H2O2-Induced Apoptosis of Intestinal Porcine Enterocyte Cells

Chen

Yuan

et al. 2018

Molecules

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Weanling stress and toxicosis, which are harmful to the health of pigs’ intestines, are associated with oxidative stress. Quercetin (Que) is a polyphenolic compound that shows good anti-cancer, anti-inflammation and anti-oxidation effects. This study aimed to elaborate whether or not Que promotes IPEC-J2 (intestinal porcine enterocyte cells) proliferation and protects IPEC-J2 from oxidative damage. Thus, we examined the effects of Que on proliferation and H2O2-induced apoptosis in IPEC-J2. The results showed that Que increased IPEC-J2 viabililty, propelled cells from G1 phase into S phase and down-regulated gene levels of P27 and P21, respectively. Besides, H2O2-induced cell damage was alleviated by Que after different exposure times, and Que depressed apoptosis rate, reactive oxygen species (ROS) level and percentage of G1 phase cells and elevated the percentage of cells in G2 phase and S phase and mitochondrial membrane potential (Δψm) after IPEC-J2 exposure to H2O2. Meanwhile, Que reduced the value of Bax/Bcl-2 in H2O2 exposed cells. In low-degree oxidative damage cells, lipid peroxidation product malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were increased. In turn, Que could reverse the change of MDA content and SOD activity in low-degree damage cells. Nevertheless, catalase (CAT) activity was not changed in IPEC-J2 incubated with Que under low-degree damage conditions. Interestingly, relative expressive levels of the proteins claudin-1 and occludin were not altered under low-degree damage conditions, but Que could improve claudin-1 and occludin levels, slightly. This research indicates that Que can be greatly beneficial for intestinal porcine enterocyte cell proliferation and it protects intestinal porcine enterocyte cells from oxidation-induced apoptosis, and could be used as a potential feed additive for porcine intestinal health against pathogenic factor-induced oxidative damages and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Effects of Quercetin on Proliferation and H2O2-Induced Apoptosis of Intestinal Porcine Enterocyte Cells

Chen

Yuan

et al. 2018

Molecules

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“…The use of medicinal plants for the treatment of diseases is gaining more popularity in the 21st century especially in Africa (Kayode & Kayode, ; Mahlangeni, Moodley, & Jonnalagadda, ) This is consequent on their various biologically active phytochemicals (Krishnaiah, Sarbatly, & Nithyanandam, ; Rahmatullah et al, ). Flavonoids mitigate free radical/oxidative stress induced tissue damage (Chen et al, ; Salem et al, ).…”

Section: Introductionmentioning

confidence: 99%

Testicular microanatomical and hormonal alterations following use of antiretroviral therapy inSprague Dawleyrats: Role of Naringenin

et al. 2018

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Human immunodeficiency virus-infected man may require assisted reproductive technology not just for safer conception but also due to subfertility. The study investigated the effect of antiretroviral drugs on the fertility potentials of males and the possible protective role of Naringenin, using Sprague Dawley rats. Thirty adult male Sprague Dawley rats were grouped into-A: Distilled water; B: Highly Active Antiretroviral Therapy (HAART); C: Naringenin 40 mg/kg; D: Naringenin 80 mg/kg, E: HAART + Naringenin 40 mg/kg; F: HAART + Naringenin 80 mg/kg. The rats were euthanised after 10 weeks. Results showed a significant decrease in sperm count in group B when compared to the control and other groups. Spermatozoa with normal morphology also reduced significantly in the B group and progressive sperm motility reduced when compared to the control, D and the F group. The serum testosterone was not significantly different between groups A and B, however the groups C and D displayed significant increase when compared to groups A and B. The serum luteinising hormone was significantly higher in group B when compared to groups A, E and F. Our data suggest that Naringenin improves the male reproductive anatomy and function, therefore, it promises to be a beneficial adjuvant for mitigating HAART testicular and reproductive perturbations.

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“…Qcn has been shown to play a fundamental role in modulating mitochondrial function by influencing ∆Ψm (Ben Salem et al, 2016 ). To determine whether Qcn also has an anti-apoptotic effect on hypoxia-induced RGC by ameliorating mitochondrial function, ∆Ψm and intracellular ROS levels were determined under hypoxia with or without Qcn.…”

Section: Resultsmentioning

confidence: 99%

“…Quercetin (Qcn) is a natural and important dietary flavonoid compound that is widely distributed in fruits and vegetables. Mounting evidence suggests that Qcn has numerous beneficial effects, including anti-inflammatory (Periasamy et al, 2016 ), anti-apoptosis (Ben Salem et al, 2016 ), anti-ischemic (Ekinci Akdemir et al, 2016 ), anti-oxidation (Xu et al, 2016 ), anti-endoplasmic reticulum (ER) stress (Ben Salem et al, 2015 ), anti-mutagenic (Barcelos et al, 2011 ), and anti-viral (Wu W. et al, 2015 ) effects in addition to promoting mitochondrial biogenesis (Sharma et al, 2015 ). In the retina, it has been reported that Qcn has protective effects in multiple lesions, including retina ischemia-reperfusion injury (Arikan et al, 2015 ), oxidative damage of RPE cells (Hytti et al, 2015 ), diabetes-induced retinal neurodegeneration (Kumar et al, 2014 ), choroidal neovascularization in age-related macular degeneration (Zhuang et al, 2011 ), vascular endothelial growth factor-induced choroidal and retinal angiogenesis (Li et al, 2015 ), and ocular inflammation (Romero et al, 1989 ).…”

Section: Introductionmentioning

confidence: 99%

Quercetin Declines Apoptosis, Ameliorates Mitochondrial Function and Improves Retinal Ganglion Cell Survival and Function in In Vivo Model of Glaucoma in Rat and Retinal Ganglion Cell Culture In Vitro

Gao

Zhang

et al. 2017

Front. Mol. Neurosci.

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Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs). Strategies that delay or halt RGC loss have been recognized as potentially beneficial for rescuing vision in glaucoma patients. Quercetin (Qcn) is a natural and important dietary flavonoid compound, widely distributed in fruits and vegetables. Mounting evidence suggests that Qcn has numerous neuroprotective effects. However, whether Qcn exerts neuroprotective effects on RGC in glaucoma is poorly understood. In this study, we investigated the protective effect of Qcn against RGC damage in a rat chronic ocular hypertension (COHT) model in vivo and hypoxia-induced primary cultured RGC damage in vitro, and we further explored the underlying neuroprotective mechanisms. We found that Qcn not only improved RGC survival and function from a very early stage of COHT in vivo, it promoted the survival of hypoxia-treated primary cultured RGCs in vitro via ameliorating mitochondrial function and preventing mitochondria-mediated apoptosis. Our findings suggest that Qcn has direct protective effects on RGCs that are independent of lowering the intraocular pressure (IOP). Qcn may be a promising therapeutic agent for improving RGC survival and function in glaucomatous neurodegeneration.

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Quercetin protects HCT116 cells from Dichlorvos-induced oxidative stress and apoptosis

Cited by 28 publications

References 45 publications

Effects of Quercetin on Proliferation and H2O2-Induced Apoptosis of Intestinal Porcine Enterocyte Cells

Effects of Quercetin on Proliferation and H2O2-Induced Apoptosis of Intestinal Porcine Enterocyte Cells

Testicular microanatomical and hormonal alterations following use of antiretroviral therapy inSprague Dawleyrats: Role of Naringenin

Quercetin Declines Apoptosis, Ameliorates Mitochondrial Function and Improves Retinal Ganglion Cell Survival and Function in In Vivo Model of Glaucoma in Rat and Retinal Ganglion Cell Culture In Vitro

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