Quercetin potentiates insulin secretion and protects INS-1 pancreatic β-cells against oxidative damage via the ERK1/2 pathway
被引:200
作者:
Youl, E.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Youl, E.
[2
]
Bardy, G.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Bardy, G.
[2
]
Magous, R.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Magous, R.
[2
]
Cros, G.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Cros, G.
[2
]
Sejalon, F.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Sejalon, F.
[2
]
Virsolvy, A.
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机构:
INSERM, CHU A de Villeneuve, U637, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Virsolvy, A.
[3
]
Richard, S.
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INSERM, CHU A de Villeneuve, U637, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Richard, S.
[3
]
Quignard, J. F.
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Univ Bordeaux 2, INSERM, U885, F-33076 Bordeaux, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Quignard, J. F.
[4
]
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机构:
Gross, R.
[2
]
Petit, P.
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机构:
Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Petit, P.
[2
]
Bataille, D.
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Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Bataille, D.
[2
]
Oiry, C.
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Fac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Univ Montpellier I, Montpellier, FranceFac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
Oiry, C.
[1
,2
]
机构:
[1] Fac Pharm Montpellier, CPID, CNRS, UMR 5232, F-34093 Montpellier 5, France
[2] Univ Montpellier I, Montpellier, France
[3] INSERM, CHU A de Villeneuve, U637, Montpellier, France
[4] Univ Bordeaux 2, INSERM, U885, F-33076 Bordeaux, France
BACKGROUND AND PURPOSE Quercetin lowers plasma glucose, normalizes glucose tolerance tests and preserves pancreatic beta-cell integrity in diabetic rats. However, its mechanism of action has never been explored in insulin-secreting beta-cells. Using the INS-1 beta-cell line, the effects of quercetin were determined on glucose- or glibenclamide-induced insulin secretion and on beta-cell dysfunctions induced by hydrogen peroxide (H2O2). These effects were analysed along with the activation of the extracellular signal-regulated kinase (ERK)1/2 pathway. N-acetyl-L-cysteine (NAC) and resveratrol, two antioxidants also known to exhibit some anti-diabetic properties, were used for comparison. EXPERIMENTAL APPROACH Insulin release was quantified by the homogeneous time resolved fluorescence method and ERK1/2 activation tested by Western blot experiments. Cell viability was estimated by the [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) colorimetric assay. KEY RESULTS Quercetin (20 mu mol.L-1) potentiated both glucose (8.3 mmol.L-1)- and glibenclamide (0.01 mu mol.L-1)- induced insulin secretion and ERK1/2 phosphorylation. The ERK1/2 (but not the protein kinase A) signalling pathway played a crucial role in the potentiation of glucose- induced insulin secretion by quercetin. In addition, quercetin (20 mu mol.L-1), protected b-cell function and viability against oxidative damage induced by 50 mu mol.L-1 H2O2 and induced a major phosphorylation of ERK1/2. In the same conditions, resveratrol or NAC were ineffective. CONCLUSION AND IMPLICATIONS Quercetin potentiated glucose and glibenclamide-induced insulin secretion and protected beta-cells against oxidative damage. Our study suggested that ERK1/2 played a major role in those effects. The potential of quercetin in preventing beta-cell dysfunction associated with diabetes deserves further investigation.