首页> 外文期刊>Journal of Ethnopharmacology: An Interdisciplinary Journal Devoted to Bioscientific Research on Indigenous Drugs >Fructus Corni suppresses hepatic gluconeogenesis related gene transcription, enhances glucose responsiveness of pancreatic beta-cells, and prevents toxin induced beta-cell death.
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Fructus Corni suppresses hepatic gluconeogenesis related gene transcription, enhances glucose responsiveness of pancreatic beta-cells, and prevents toxin induced beta-cell death.

机译:山茱Corn抑制肝糖原异生相关基因的转录,增强胰腺β细胞的葡萄糖反应能力,并防止毒素诱导的β细胞死亡。

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摘要

ETHNOPHARMACOLOGICAL RELEVANCE: Fructus Corni, the fruits of Cornus officinalis Sieb. et Zucc., is one important ingredient in Quei Fu Di Huang Wan, a Chinese herbal mixture. AIM OF THE STUDY: In the present study, additional anti-diabetic actions of Fructus Corni on transcriptional regulation of hepatic gluconeogenesis or beta-cell functions were investigated. MATERIALS AND METHODS: Insulin mimetic action of Fructus Corni on dexamethasone and 8-bromo-cAMP induced phosphoenolpyruvate carboxykinase (PEPCK) expression in H4IIE cells was investigated. Besides, BRIN-BD11 cells were used to evaluate both insulinotropic and beta-cell protective effect of Fructus Corni. RESULTS: Firstly, both methanol extract (CO-W-M) and fraction (CO-W-M2) had potent insulin mimic activity on PEPCK expression. Secondly, possibility of both loganin and ursolic acid as the responsible compounds was excluded. Moreover, indication of the existence of phenolic compounds in CO-W-M2 was noticed. In the presence of CO-W-M2, not onlywas the viability of BRIN-BD11 cells treated with alloxan, streptozotcin, or cytokine mix all significantly increased but also glucose-stimulated insulin secretion was potentiated. CONCLUSIONS: The ability of CO-W-M2 to reduce gene expression for hepatic gluconeogenesis, to protect beta-cell against toxic challenge, and to enhance insulin secretion strengthen the role of Fructus Corni in diabetes therapy.
机译:人种药理关系:山茱F,山茱off的果实。 et Zucc。是中草药混合物Quei Fu Di Huang Wan的一种重要成分。研究目的:在本研究中,研究了山茱F对肝糖异生或β细胞功能的转录调控的其他抗糖尿病作用。材料与方法:研究山茱F对H4IIE细胞中地塞米松和8-溴-cAMP诱导的磷酸烯醇丙酮酸羧化激酶(PEPCK)表达的胰岛素模拟作用。此外,使用BRIN-BD11细胞评估山茱ru的促胰岛素作用和β细胞保护作用。结果:首先,甲醇提取物(CO-W-M)和馏分(CO-W-M2)对PEPCK表达均具有有效的胰岛素模拟活性。其次,排除了以鼠李糖苷和熊果酸作为负责化合物的可能性。而且,注意到在CO-W-M2中存在酚类化合物的迹象。在存在CO-W-M2的情况下,不仅用四氧嘧啶,链脲佐菌素或细胞因子混合物处理过的BRIN-BD11细胞的活力都显着增加,而且葡萄糖刺激的胰岛素分泌也得到了增强。结论:CO-W-M2减少肝糖异生的基因表达,保护β细胞免受毒性攻击,增强胰岛素分泌的能力增强了山茱F在糖尿病治疗中的作用。

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