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机构地区:[1]江西省果蔬保鲜与无损检测重点实验室、江西农业大学农学院,江西南昌330045 [2]三峡大学医学院,湖北宜昌443002 [3]江西中医药大学附属医院,江西南昌330006
出 处:《现代食品科技》2017年第9期96-101,共6页Modern Food Science and Technology
基 金:国家自然科学基金青年科学基金项目(31500286);江西省青年科学基金项目(20161BAB214167)资助
摘 要:为研究余甘子提取物的降血糖作用机制,本文研究了其对LO2细胞葡萄糖转运蛋白2(GLUT-2)和过氧化物酶体增殖物激活受体-γ(PPARγ)m RNA表达及过氧化物酶体增殖物反应元件(PPER)和核转录因子kappa B(NF-κB)活性的影响。该实验采用D101大孔树脂柱对余甘子提取物进行初步分离,得到三个组分;采用Real-Time PCR和荧光素酶报告基因方法研究余甘子提取物及其有效组分对GLUT-2和PPARγm RNA表达和PPER和NF-κB荧光素酶活性。余甘子提取物可以显著升高GLUT-2和PPARγm RNA的表达和PPRE报告基因的活性,抑制脂多糖(LPS)诱导的炎症反应,可以降低NF-κB报告基因的活性,随着浓度的升高其抑制作用增强。大孔树脂柱30%乙醇洗脱物为其有效活性组分。通过Sephadex LH-20,ODS和制备HPLC等柱色谱技术分离鉴定了一个主要的成分为没食子酸;余甘子可能是通过升高GLUT-2和PPARγ的表达和抑制相关炎症通路发挥降血糖作用,没食子酸可能为其主要的活性成分。The effects of Phyllanthus emblica L extract on mRNA expressions of GLUT-2 (glucose transporter type 2) and PPAR7 (peroxisome proliferator-activated receptor-γ) and the activities of PPRE (peroxisome proliferator response element) and NF-κB in LO2 cells were studied to elucidate the hypoglycemic mechanism and the main active components of this extract. The methanol extracts of P emblica L were first isolated using a D101 macroporous resin column to yield three fractions. Real-time polymerase chain reaction (PCR) and luciferase reporter gene methods were applied to study the effects of the extracts ofP emblica L and their active components on the mRNA expressions of GLUT-2 and PPARγ, and the activities of PPRE and NF-κB. The extracts of P emblica L significantly enhanced the mRNA expression of GLUT-2 and PPARγ and activity of the PPRE reporter gene (p〈0.05), inhibited the lipopolysaccharide (LPS)-induced inflammation (p〈0.05), and reduced the activity of the NF-κB reporter gene; the inhibitory effect was dose-dependent (p〈0.05). The 30% ethanol-eluted fraction from the macroporous resin column was the active fi'action. Sephadex LH-20, C 18 (ODS), semi-preparative high performance liquid chromatography (HPLC) columns were used, and one main component was isolated and identified as gallic acid. P emblica L might exert its hypoglycemic effect by increasing the expressions of GLUT-2 and PPARγ and inhibiting the inflammation-related pathway. Gallic acid may be the major active component.
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