EGCG and quercetin protected INS-1 cells in oxidative stress via different mechanisms

Kim, Mi K.; Jung, Hwa Jin; Yoon, Chang Shin; Ko, Jeong Heon; Chun, Hye Jeong; Kim, Tae Kyoung; Kwon, Min Jeong; Lee, Soon H; Koh, Kyung Soo; Rhee, Byung Doo; Park, Jeong H.

doi:10.2741/e142

Cited by 24 publications

(3 citation statements)

References 33 publications

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“…EGCG can prevent abnormal changes in blood glucose and lipid profile and attenuate hepatic lipid peroxidation in STZ-induced diabetic rats [111]. EGCGs have protective effect on the insulinoma-1 (INS-1) beta cells against oxidative stress both through antioxidant effect and antiapoptotic signalling [112]. EGCG inhibits ERK and activates AMPK [113].…”

Section: Compounds Derived From Tcmmentioning

confidence: 99%

Diabetes is an inflammatory disease: evidence from traditional Chinese medicines

Xie

2011

Diabetes, Obesity and Metabolism

275

182

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Diabetes is usually associated with inflammation. Inflammation contributes to the development of diabetes. Traditional Chinese medicines (TCM) play an important role in lowering blood glucose and controlling inflammation. Many studies show that TCM with hypoglycaemic effects, for example Radix Astragali, Radix Rehmanniae, Radix Trichosanthis, Panax Ginseng, Fructus Schisandrae, Radix Ophiopogonis, Rhizoma Anemarrhenae, Radix Puerariae, Fructus Lycii, Poria, Rhizoma Coptidis, Rhizoma Dioscoreae, Rhizoma Polygonati, Radix Salviae Miltiorrhizae, Radix Glycyrrhizae, Semen Trigonellae, Momordica charantia, Allium sativum, Opuntia stricta, Aloe vera, Cortex Cinnamomi, Rhizoma Curcumae Longae, and so on, have nearly independent anti-inflammatory action. Antihyperglycaemic compounds, for example berberine, puerarin, quercetin, ferulic acid, astragaloside IV, curcumin, epigallocatechin gallate, resveratrol, tetrandrine, glycyrrhizin, emodin and baicalin, used in TCM also have anti-inflammatory effects. These studies suggest that TCM might exert hypoglycaemic effects that are partly mediated by the anti-inflammatory mechanisms. However, small amounts of TCM with potent anti-inflammatory action does not have any hypoglycaemic effect. This indirectly indicates that diabetes may be a low-grade inflammatory disease and potent regulation of inflammatory mediators may not be required. Studies of TCM add new evidences, which indicate that diabetes may be an inflammatory disease and slight or moderate inhibition of inflammation might be useful to prevent the development of diabetes. Through this review, we aim to develop more perspectives to indicate that diabetes may be an inflammatory disease and diverse TCM may share a common antidiabetic property: anti-inflammatory action. Further studies should focus on and validate inflammation-regulating targets of TCM that may be involved in inhibiting the development of diabetes.

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Section: Compounds Derived From Tcmmentioning

confidence: 99%

Diabetes is an inflammatory disease: evidence from traditional Chinese medicines

Xie

2011

Diabetes, Obesity and Metabolism

275

182

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“…Quercetin also has been shown to induce apoptosis by releasing cytochrome c and activating caspase-9 and caspase-3 [60-62]. Moreover, quercetin is believed to be a potential PI3K inhibitor, an enzyme involved in the pivotal cell survival pathway [63,64]. Interestingly, quercetin has been shown to enhance the anticancer activities of several chemotherapeutic drugs and inhibit the expression of P-glycoprotein [65-70].…”

Section: Introductionmentioning

confidence: 99%

The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition

Tang¹,

Singh²,

Nall³

et al. 2010

JMS

193

128

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BackgroundMuch attention has been recently focused on the role of cancer stem cells (CSCs) in the initiation and progression of solid malignancies. Since CSCs are able to proliferate and self-renew extensively due to their ability to express anti-apoptotic and drug resistant proteins, thus sustaining tumor growth. Therefore, the strategy to eradicate CSCs might have significant clinical implications. The objectives of this study were to examine the molecular mechanisms by which epigallocathechin gallate (EGCG) inhibits stem cell characteristics of prostate CSCs, and synergizes with quercetin, a major polyphenol and flavonoid commonly detected in many fruits and vegetables.ResultsOur data indicate that human prostate cancer cell lines contain a small population of CD44+CD133+ cancer stem cells and their self-renewal capacity is inhibited by EGCG. Furthermore, EGCG inhibits the self-renewal capacity of CD44+α2β1+CD133+ CSCs isolated from human primary prostate tumors, as measured by spheroid formation in suspension. EGCG induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2, survivin and XIAP in CSCs. Furthermore, EGCG inhibits epithelial-mesenchymal transition by inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter, and also retards CSC's migration and invasion, suggesting the blockade of signaling involved in early metastasis. Interestingly, quercetin synergizes with EGCG in inhibiting the self-renewal properties of prostate CSCs, inducing apoptosis, and blocking CSC's migration and invasion. These data suggest that EGCG either alone or in combination with quercetin can eliminate cancer stem cell-characteristics.ConclusionSince carcinogenesis is a complex process, combination of bioactive dietary agents with complementary activities will be beneficial for prostate cancer prevention and/ortreatment.

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“…Kagaya et al (30) observed that zinc was able to enhance the hepatoprotective effects of EGCG in isolated rat hepatocytes, and it has also been reported that exogenous zinc protects cardiomyocytes against H/R-induced apoptosis by targeting the PI3k/Akt pathway (18). In addition, previous studies have observed that the pretreatment with EGCG had protective effect on INS-1 cells against oxidative stress via the enhancement of anti-apoptosis signaling through increased levels of phosphorylated PI3K and Akt (31). The effects of EGCG on PI3K/Akt signaling in myoctyes remain to be fully elucidated, and little is known about the actions of EGCG + Zn 2+ on H/R-induced H9c2 cell growth and apoptosis and the associated intracellular signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate and zinc provide anti-apoptotic protection against hypoxia/reoxygenation injury in H9c2 rat cardiac myoblast cells

Zeng

Tan

2015

Molecular Medicine Reports

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It has previously been demonstrated that phospha-tidylinositol-3-kinase (PI3K)/Akt and cleaved caspase-3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. Epigallocatechin-3-gallate (EGCG), the predominant catechin component of green tea, has been reported to have potential cardioprotective effects in primary cultures of cardiac myocytes exposed to I/R injury, mediated through inhibition of signal transducers and activators of transcription-1 activity. In addition, it is also known that the biological behavior of EGCG may be influenced by metal ions, for example the hepatoprotective activity of EGCG has been reported to be enhanced by zinc. In the present study, the protective effects of EGCG with zinc were assessed on cultures of rat cardiac myoblasts exposed to hypoxia/reoxygenation (H/R) injury. H9c2 cells were subjected to 3-h hypoxia, followed by 1-h reperfusion. EGCG and/or zinc were perfused prior to induced hypoxic stress. It was demonstrated that when EGCG interacted with zinc, the anti-apoptotic activity was significantly enhanced. To the best of our knowledge, the current study was the first to demonstrate that EGCG + Zn2+ protects H9c2 cells against H/R injury through activation of the PI3K/Akt pathway, as determined by western blotting. Since EGCG + Zn2+ may, at least in part, protect cardiac myocytes against H/R-induced apoptotic cell death, the PI3K/Akt pathway of EGCG may be enhanced by its interactions with zinc during H/R injury. Furthermore, it was suggested that a similar procedure may be implemented in a clinical setting, in order to maximize PI3K/Akt activation levels in patients with acute coronary artery disease. EGCG and zinc may therefore represent effective agents for use in the prevention of I/R injury in clinical practice.

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EGCG and quercetin protected INS-1 cells in oxidative stress via different mechanisms

Cited by 24 publications

References 33 publications

Diabetes is an inflammatory disease: evidence from traditional Chinese medicines

Diabetes is an inflammatory disease: evidence from traditional Chinese medicines

The dietary bioflavonoid quercetin synergizes with epigallocathechin gallate (EGCG) to inhibit prostate cancer stem cell characteristics, invasion, migration and epithelial-mesenchymal transition

Epigallocatechin-3-gallate and zinc provide anti-apoptotic protection against hypoxia/reoxygenation injury in H9c2 rat cardiac myoblast cells

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