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Zhonghua Yi Xue Za Zhi. 2012 Mar 13;92(10):695-9.

[1α, 25(OH)(2) D(3) protects pancreatic β-cell line from cytokine-induced apoptosis and impaired insulin secretion].

[Article in Chinese]

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Diabetes Center, Second Xiangya Hospital & Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha 410011, China.



To explore the protective effects and potential mechanisms of 1α, 25(OH)(2) D(3) (VitD(3)) on pancreatic β-cells.


The apoptosis of NIT-1 cells was induced by interleukin-1β (IL-1β) and interferon-γ (IFN-γ) in vitro. Then the apoptotic rate of NIT-1 cells was determined by Hoechest33342 staining and Annexin V-FITC/PI flow cytometry. The insulin secretion level of NIT-1 cells was measured by ELISA. The NIT-1 cells were treated with VitD(3) at the final concentrations of 10(-8) mol/L or underwent transient transfection with vitamin D receptor (VDR)-SiRNA.


After the treatment of VitD(3), the apoptotic rate of NIT-1 cells decreased to 39.7%. There were significant differences in apoptotic rate between the VitD(3) treatment and IL-1β/IFN-γ groups (68.4%) (P < 0.01). Similarly impaired glucose-stimulated insulin secretion (GSIS) of NIT-1 cells recovered ((7.34 ± 0.21) ng/ml) after the treatment of VitD(3) as compared with the IL-1β/IFN-γ group ((4.88 ± 0.32) ng/ml, P < 0.01). Moreover, most of the protective effects of VitD(3) on pancreatic β-cells could be blocked by the transfection of VDR-SiRNA.


VitD(3) may protect pancreatic β-cells from cytokine-induced apoptosis and impaired insulin secretion through its conjugation with VDR.

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