Abstract

Aims

This study was performed to explore the possible beneficial effects of vitexin on high glucose (HG)-induced cytotoxicity in pancreatic β-cells.

Methods

INS-1 pancreatic β-cell line has used this study. HG-induced (33 Mm) exposed INS-1 cell death; the apoptosis INS-1 cells treated vitexin 10, 20, 40, and 80 µg/mL for 24 hours. The anti-apoptosis properties were evaluated by MTT assay, glucose-stimulated insulin secretion assay, biochemical assay, annexin-V-FITC staining and western blot analysis.

Results

These findings demonstrate that vitexin treatment improved the HG-exposure, reduced the INS-1 cell viability and significantly enhanced glucose-stimulated insulin secretion in a dose-dependent manner. The antioxidant studies revealed that vitexin treatment significantly decreased lipid peroxidation and reactive oxygen species and increased antioxidant level of INS-1 cell line in 24 hrs. The findings of the study suggested that in the vitexin treatment group, pancreatic apoptosis and Bax protein expression reduced significantly. At the same time, Bcl-2 protein expression increased, and NF-κB protein in HG-induced INS-cells was inhibited.

Conclusion

Therefore, our results suggest that vitexin can be successfully used to regulate the expression of Bcl-2 family proteins, reduce lipid peroxidation and to improve the secretion of antioxidants in pancreatic β-cell lines.

中文翻译：

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使用牡荆素通过 INS-1 细胞凋亡保护 β-胰腺细胞免受胰岛素功能障碍的影响

摘要

目标

本研究旨在探讨牡荆素对高葡萄糖 (HG) 诱导的胰腺 β 细胞细胞毒性的可能有益影响。

方法

本研究使用了 INS-1 胰腺 β 细胞系。HG 诱导 (33 Mm) 暴露的 INS-1 细胞死亡；凋亡 INS-1 细胞用牡荆素 10、20、40 和 80 µg/mL 处理 24 小时。通过MTT测定、葡萄糖刺激胰岛素分泌测定、生化测定、膜联蛋白-V-FITC染色和蛋白质印迹分析评估抗凋亡特性。

结果

这些发现表明，牡荆素治疗改善了 HG 暴露，降低了 INS-1 细胞活力，并以剂量​​依赖性方式显着增强了葡萄糖刺激的胰岛素分泌。抗氧化研究表明，牡荆素处理在 24 小时内显着降低了 INS-1 细胞系的脂质过氧化和活性氧，并提高了抗氧化水平。研究结果表明，在牡荆素治疗组中，胰腺细胞凋亡和Bax蛋白表达显着减少。同时，HG诱导的INS细胞中Bcl-2蛋白表达增加，NF-κB蛋白表达受到抑制。

结论

因此，我们的结果表明牡荆素可成功用于调节 Bcl-2 家族蛋白的表达，减少脂质过氧化并改善胰腺 β 细胞系抗氧化剂的分泌。