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食物来源的山奈酚对1型糖尿病患者胰腺β细胞的保护作用

Protective Effects of Food-Derived Kaempferol on Pancreatic β-Cells in Type 1 Diabetes Mellitus.

作者信息

Song Chenmeng, Zheng Wei, Song Chengyi, Zhou Houfeng, Yao Jengyuan

机构信息

School of Public Health, Fujian Medical University, Fuzhou 350005, China.

Department of Pharmacy, Xiamen Medical College, Xiamen 361005, China.

出版信息

Foods. 2024 Nov 26;13(23):3797. doi: 10.3390/foods13233797.

Abstract

BACKGROUND

Kaempferol (KPF), a flavonoid abundant in edible plants, possesses potent anti-inflammatory and antioxidant properties beneficial with notable health benefits.

OBJECTIVE

To evaluate the protective effects of KPF on metabolic disturbances and pancreatic damage in a Type 1 diabetes mellitus (T1DM) mouse model.

METHODS

Male C57BL/6 mice were divided into normal, T1DM, T1DM + KPF 25 mg/kg, and T1DM + KPF 50 mg/kg groups. T1DM was induced by streptozotocin (STZ). KPF was administered via intraperitoneal injection for 2 weeks. After 4 weeks from the start, metabolic parameters, pancreatic histology, and plasma metabolites were analyzed. Network pharmacology and molecular docking identified key targets and pathways. In vitro, INS-1 cells were used to assess reactive oxygen species (ROS) production and apoptosis.

RESULTS

KPF significantly reduced blood glucose (GLU) and triglyceride (TG) levels, increased high-density lipoprotein (HDL) levels, and preserved pancreatic β-cell structure. Metabolomics revealed changes in energy metabolism and oxidative stress-related metabolites. Network analysis highlighted the PI3K/AKT/mTOR pathway, with strong binding affinities to targets such as AKT1. In vitro, KPF decreased ROS production in INS-1 cells; this effect was reversed by a PI3K/AKT inhibitor. KPF also reduced apoptosis in INS-1 cells.

CONCLUSIONS

KPF ameliorates metabolic disturbances and pancreatic damage in T1DM mice, suggesting potential as a functional food ingredient for diabetes management.

摘要

背景

山奈酚(KPF)是一种在可食用植物中含量丰富的黄酮类化合物,具有强大的抗炎和抗氧化特性,对健康有益。

目的

评估山奈酚(KPF)对1型糖尿病(T1DM)小鼠模型代谢紊乱和胰腺损伤的保护作用。

方法

将雄性C57BL/6小鼠分为正常组、T1DM组、T1DM + 25 mg/kg KPF组和T1DM + 50 mg/kg KPF组。通过链脲佐菌素(STZ)诱导T1DM。通过腹腔注射给予KPF,持续2周。从开始4周后,分析代谢参数、胰腺组织学和血浆代谢物。网络药理学和分子对接确定关键靶点和途径。在体外,使用INS-1细胞评估活性氧(ROS)产生和细胞凋亡。

结果

KPF显著降低血糖(GLU)和甘油三酯(TG)水平,提高高密度脂蛋白(HDL)水平,并保留胰腺β细胞结构。代谢组学揭示了能量代谢和氧化应激相关代谢物的变化。网络分析突出了PI3K/AKT/mTOR途径,与AKT1等靶点具有强结合亲和力。在体外,KPF降低了INS-1细胞中的ROS产生;PI3K/AKT抑制剂可逆转这种作用。KPF还减少了INS-1细胞中的细胞凋亡。

结论

KPF改善了T1DM小鼠的代谢紊乱和胰腺损伤,表明其作为糖尿病管理功能性食品成分的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e0/11640530/efad296d0ffe/foods-13-03797-g001.jpg

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