1-deoxynojirimycin通过调节CEBPA表达和AMPK通路来影响高葡萄糖诱导的胰腺β细胞功能障碍
Xiaoying Li1, Shenggui Liu1, Siqi Wang2
1Key Laboratory of Research and Utilization of Ethnomedicinal Plant Resources of Hunan Province, College of Biology and Food Engineering, Huaihua University, Huaihua 418000, Hunan, China.
Biochemistry and cell biology = Biochimie et biologie cellulaire
|November 15, 2024
概括
1-deoxynojirimycin (DNJ) 保护胰腺β细胞免受高葡萄糖损伤. DNJ促进CEBPA的表达,恢复正常的细胞功能和胰岛素分泌.
科学领域:
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 高血糖水平诱导胰腺β细胞功能障碍,损害胰岛素分泌,促进细胞亡.
- 了解这种功能障碍背后的分子机制对于开发治疗策略至关重要.
研究的目的:
- 为了研究1-deoxynojirimycin (DNJ) 对高葡萄糖诱导的β细胞功能障碍的保护作用.
- 通过网络药理学阐明DNJ对β细胞影响的分子机制.
主要方法:
- 鼠标INS-1β细胞被用高葡萄糖和/或DNJ治疗.
- 评估了细胞增殖,胰岛素分泌,亡标志物 (裂开的酶-3,-9),活性氧物种 (ROS) 和CEBPA表达.
- 为了评估其在β细胞功能障碍中的作用,CEBPA被沉默或过度表达.
主要成果:
- 高葡萄糖损害了INS-1细胞增殖和胰岛素分泌,增加了细胞亡和ROS产生,并降低了Bcl-2表达.
- DNJ治疗逆转了高葡萄糖诱导的β细胞功能障碍,对正常细胞没有毒性.
- 沉默CEBPA加剧了高葡萄糖引起的功能障碍,而它的过度表达减轻了它.
- 在CEBPA沉默细胞中,DNJ部分恢复了β细胞功能.
结论:
- 1-deoxynojirimycin (DNJ) 保护胰腺β细胞免受高葡萄糖诱导的功能障碍.
- DNJ通过促进CEBPA表达来发挥其保护作用,从而恢复β细胞功能.
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