Prooxidative effects of green tea polyphenol (−)-epigallocatethin-3-gallate on the HIT-T15 pancreatic beta cell line

Suh, Kwang Sik; Chon, Suk; Oh, Seungjoon; Kim, Sung Woon; Kim, Jin-Woo; Kim, Young Seol; Woo, Jeong-Taek

doi:10.1007/s10565-009-9137-7

Cited by 64 publications

(61 citation statements)

References 35 publications

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“…Although ROS act as signal transducers, when accumulated in cells in the form of hydrogen peroxide, superoxide, and hydroxyl radicals, ROS are considered essential regulators of aging and have been reported to be a key element in the apoptosis of yeast (48)(49)(50). The synergistic interactions observed in this study indicate a probable prooxidant activity of flavonoids, which may be responsible for the induction of transcription factors associated with apoptosis and related to increased levels of proapoptotic proteins, mitochondrial injury, and ROS generation, as well as accelerated oxidative damage to DNA, proteins, and carbohydrates in vitro (51)(52)(53).…”

Section: Figmentioning

confidence: 62%

“…Such a ⌬m collapse can lead to transient pore openings in the mitochondrial membrane and the release of proapoptotic factors into the cytosol (50,54). This fact can be explained by the ability of flavonoids to exhibit a prooxidant activity (52,53) that favors increased intracellular levels of hydroxyl radicals that lead to mitochondrial membrane damage. Hwang et al (55) showed that the flavonoid amentoflavone promotes mitochondrial dysfunction in C. albicans strains due to increased levels of ROS.…”

Section: Figmentioning

confidence: 99%

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Synergistic Effect of the Flavonoid Catechin, Quercetin, or Epigallocatechin Gallate with Fluconazole Induces Apoptosis in Candida tropicalis Resistant to Fluconazole

Silva

Neto

Campos

et al. 2014

Antimicrob Agents Chemother

107

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Section: Figmentioning

confidence: 62%

Section: Figmentioning

confidence: 99%

Synergistic Effect of the Flavonoid Catechin, Quercetin, or Epigallocatechin Gallate with Fluconazole Induces Apoptosis in Candida tropicalis Resistant to Fluconazole

Silva

Neto

Campos

et al. 2014

Antimicrob Agents Chemother

107

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“…We have shown previously that the antioxidants NAC and ALA protect pancreatic β-cells and MC3T3-E1 osteoblastic cells against oxidative stress as shown by a reduction in ROS generation and apoptosis. [14][15][16]19,31) These findings indicate that apigenin can function as an antioxidant and thereby protect pancreatic β-cells from dRib-induced oxi- dative cell damage. We used JC-1 staining to assess ΔΨ m, which is a marker of mitochondrial oxidative phosphorylation activity.…”

Section: Resultsmentioning

confidence: 88%

Apigenin Attenuates 2-Deoxy-D-ribose-Induced Oxidative Cell Damage in HIT-T15 Pancreatic .BETA.-Cells

Suh

Woo

et al. 2012

Biological & Pharmaceutical Bulletin

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Glucose toxicity contributes to progressive β-cell failure and the development of overt diabetes. Oxidative stress is an important aspect of glucose toxicity in pancreatic β-cells. We investigated whether the flavonoid apigenin protects pancreatic β-cells from 2-deoxy-D-ribose (dRib)-induced oxidative cell damage. HIT-T15 pancreatic β-cells were cultured with or without apigenin in the presence of dRib. Time-and dosedependent cell viability was monitored using a cell counting kit (CCK-8), while the induction of apoptosis was analyzed using a cell death enzyme-linked immunosorbent assay (ELISA) kit. Mitochondrial membrane potential (ΔΨ m ) was determined using the JC-1 kit. Intracellular oxidative stress was measured by fluorometric analysis of DCFH oxidation using 2′,7′-dichlorofluorescin diacetate (DCFH-DA) as the probe. In addition, the DNA binding activity of the oxidative stress-related transcriptional factors nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) were analyzed. dRib reduced cell survival and ΔΨ m , while it markedly increased intracellular levels of reactive oxygen species (ROS), apoptosis, and the activity of the oxidative stress-related transcription factors NF-κB and AP-1. However, pretreatment of cells with apigenin attenuated all the dRib-induced effects. The anti-oxidants, N-acetyl-L-cysteine (NAC) and alpha lipoic acid (ALA), also prevented both dRib-induced oxidative damage and activation of NF-κB and AP-1. Taken together, these results suggest that apigenin attenuates dRib-induced cell damage in pancreatic β-cells via oxidative stressrelated signaling. Key words oxidative stress; apigenin; 2-deoxy-D-ribose; diabetes; pancreatic β-cellOxidative stress is known to be a major contributor to the development of overt diabetes and its associated complications.1) Oxidative stress results from a persistent imbalance between antioxidant defenses and the production of highly reactive oxygen species (ROS).2) ROS are normal byproducts of cellular metabolism. However, a marked increase in glucose metabolism could lead to excessive ROS production, which could contribute to the development of diabetic complications. In particular, pancreatic β-cells express low levels of antioxidant enzymes and do not up-regulate these enzymes upon exposure to high concentrations of glucose.3) Thus, increased ROS production in the presence of low antioxidant defense levels could result in ROS accumulation, which would lead to the oxidative pancreatic β-cell damage that is partly responsible for diabetes. Nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) are 2 redox-sensitive transcription factors that can be regulated by oxidative stress. [4][5][6] By activating these transcription factors in isolated peripheral mononuclear cells of diabetic patients, ROS are also involved in the pathogenesis of diabetic nephropathy. 7) In addition, activation of NF-κB correlates with the quality of glycemic control and has been shown to be reduced by treatment with antioxidants in a diabetic animal model and diabetic pa...

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“…Intracellular reactive oxygen species (ROS) levels were measured using Image-iT LIVE Green Reactive Oxygen Species Detection Kit (Molecular Probes, Life Technologies Europe BV) as described previously (Suh et al 2010). Briefly, the assay is based on 5-(and-6)-carboxy-2 0 , 7 0 -dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA), a fluorogenic marker that will be cleaved upon the presence of ROS.…”

Section: Measurement Of Intracellular Reactive Oxygen Speciesmentioning

confidence: 99%

Exendin-4 protects endothelial cells from lipoapoptosis by PKA, PI3K, eNOS, p38 MAPK, and JNK pathways

Erdogdu

Eriksson

et al. 2013

Journal of Molecular Endocrinology

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Experimental studies have indicated that endothelial cells play an important role in maintaining vascular homeostasis. We previously reported that human coronary artery endothelial cells (HCAECs) express the glucagon-like peptide 1 (GLP1) receptor and that the stable GLP1 mimetic exendin-4 is able to activate the receptor, leading to increased cell proliferation. Here, we have studied the effect of exendin-4 and native GLP1 (7-36) on lipoapoptosis and its underlying mechanisms in HCAECs. Apoptosis was assessed by DNA fragmentation and caspase-3 activation, after incubating cells with palmitate. Nitric oxide (NO) and reactive oxidative species (ROS) were analyzed. GLP1 receptor activation, PKA-, PI3K/Akt-, eNOS-, p38 MAPK-, and JNK-dependent pathways, and genetic silencing of transfection of eNOS were also studied. Palmitate-induced apoptosis stimulated cells to release NO and ROS, concomitant with upregulation of eNOS, which required activation of p38 MAPK and JNK. Exendin-4 restored the imbalance between NO and ROS production in which ROS production decreased and NO production was further augmented. Incubation with exendin-4 and GLP1 (7-36) protected HCAECs against lipoapoptosis, an effect that was blocked by PKA, PI3K/Akt, eNOS, p38 MAPK, and JNK inhibitors. Genetic silencing of eNOS also abolished the anti-apoptotic effect afforded by exendin-4. Our results support the notion that GLP1 receptor agonists restore eNOS-induced ROS production due to lipotoxicity and that such agonists protect against lipoapoptosis through PKA-PI3K/Akt-eNOS-p38 MAPK-JNK-dependent pathways via a GLP1 receptor-dependent mechanism.

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Prooxidative effects of green tea polyphenol (−)-epigallocatethin-3-gallate on the HIT-T15 pancreatic beta cell line

Cited by 64 publications

References 35 publications

Synergistic Effect of the Flavonoid Catechin, Quercetin, or Epigallocatechin Gallate with Fluconazole Induces Apoptosis in Candida tropicalis Resistant to Fluconazole

Synergistic Effect of the Flavonoid Catechin, Quercetin, or Epigallocatechin Gallate with Fluconazole Induces Apoptosis in Candida tropicalis Resistant to Fluconazole

Apigenin Attenuates 2-Deoxy-D-ribose-Induced Oxidative Cell Damage in HIT-T15 Pancreatic .BETA.-Cells

Exendin-4 protects endothelial cells from lipoapoptosis by PKA, PI3K, eNOS, p38 MAPK, and JNK pathways

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