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肉桂皮提取物的乙酸乙酯部分可保护胰腺β细胞免受氧化应激损伤。

Ethyl-acetate fraction from a cinnamon-cortex extract protects pancreatic β-cells from oxidative stress damage.

作者信息

Li Weiling, Qiao Jialu, Lin Kuan, Sun Ping, Wang Yuansong, Peng Qian, Ye Xiansheng, Liu Wei, Sun Binlian

机构信息

School of Medicine, Wuhan Institute of Biomedical Sciences, Jianghan University, Wuhan, China.

出版信息

Front Pharmacol. 2023 Mar 6;14:1111860. doi: 10.3389/fphar.2023.1111860. eCollection 2023.

DOI:10.3389/fphar.2023.1111860
PMID:36950010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10025376/
Abstract

The pathogenesis of diabetes mellitus is mediated mainly by oxidative stress produced by damaged pancreatic β-cells. We identified that an ethyl-acetate fraction (EA) from a cinnamon-cortex extract (CCE) is rich in flavonoid, and showed no toxicity to β cells. In this study, we evaluated the pharmacologic activities of EA on pancreatic β cells using a model of oxidative stress induced by HO or alloxan. The results showed that EA could significantly reduce reactive oxygen (ROS) accumulation to improve the survival of cells. Western blot showed that EA treatment upregulated expression of nuclear factor erythroid 2 related factor 2, heme oxygenase-1, and gamma glutamylcysteine synthetase. The same model study found that EA also can protect β cells against the apoptosis induced by oxidative stress. Furthermore, EA can enhance insulin secretion in rat and mouse β cell lines treated or not with alloxan or HO. The expression of the insulin transcription factor PDX-1 increased in an EA concentration-dependent manner. At last, the major functional compounds of EA analysis showed that three compounds, cinnamyl alcohol, coumarin, and cinnamic acid, had similar effects as EA. In sum, our data suggested that EA fraction from CCE can protect β cells from oxidative stress, and increase insulin secretion to improve the function of β cells. This function might be due to these three compounds found in EA. Our findings provide a theoretical basis and functional molecules for the use of CCE against diabetes mellitus.

摘要

糖尿病的发病机制主要由受损胰腺β细胞产生的氧化应激介导。我们发现肉桂皮提取物(CCE)中的乙酸乙酯馏分(EA)富含黄酮类化合物,且对β细胞无毒性。在本研究中,我们使用HO或四氧嘧啶诱导的氧化应激模型评估了EA对胰腺β细胞的药理活性。结果表明,EA可显著减少活性氧(ROS)积累,从而提高细胞存活率。蛋白质免疫印迹法显示,EA处理上调了核因子红细胞2相关因子2、血红素加氧酶-1和γ-谷氨酰半胱氨酸合成酶的表达。同一模型研究发现,EA还可保护β细胞免受氧化应激诱导的细胞凋亡。此外,EA可增强经四氧嘧啶或HO处理或未处理的大鼠和小鼠β细胞系中的胰岛素分泌。胰岛素转录因子PDX-1的表达呈EA浓度依赖性增加。最后,对EA主要功能化合物的分析表明,肉桂醇、香豆素和肉桂酸这三种化合物具有与EA相似的作用。总之,我们的数据表明,CCE中的EA馏分可保护β细胞免受氧化应激,并增加胰岛素分泌以改善β细胞功能。该功能可能归因于EA中发现的这三种化合物。我们的研究结果为使用CCE治疗糖尿病提供了理论依据和功能分子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/e649d4769cc2/fphar-14-1111860-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/882a5aab119d/fphar-14-1111860-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/e649d4769cc2/fphar-14-1111860-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/882a5aab119d/fphar-14-1111860-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/b4ee6336b12e/fphar-14-1111860-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5415/10025376/8e85b7d6f72f/fphar-14-1111860-g003.jpg
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本文引用的文献

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Front Physiol. 2022 Nov 24;13:960580. doi: 10.3389/fphys.2022.960580. eCollection 2022.
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A Synopsis of the Associations of Oxidative Stress, ROS, and Antioxidants with Diabetes Mellitus.氧化应激、活性氧和抗氧化剂与糖尿病关联概述
Antioxidants (Basel). 2022 Oct 10;11(10):2003. doi: 10.3390/antiox11102003.
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Ethnomedicinal Plants with Protective Effects against Beta-Amyloid Peptide (Aβ)1-42 Indicate Therapeutic Potential in a New In Vivo Model of Alzheimer's Disease.
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Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management.氧化应激介导的β细胞死亡和功能障碍作为糖尿病管理的靶点。
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