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关于麦冬多糖提取物降血糖活性的机制研究。

Mechanistic studies on the antidiabetic activity of a polysaccharide-rich extract of Radix Ophiopogonis.

机构信息

School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, PR China.

出版信息

Phytother Res. 2012 Jan;26(1):101-5. doi: 10.1002/ptr.3505. Epub 2011 May 11.

DOI:10.1002/ptr.3505
PMID:21560174
Abstract

To study the hypoglycemic mechanisms of a polysaccharide-rich extract of Radix Ophiopogonis, the influences of the extract on activity of NIT-1 insulinoma cells damaged by streptozotocin (STZ), activity of α-glucosidase, glucose absorption into intestinal brush border membrane vesicles, gluconeogenesis by H4IIE hepatoma cells and glucose uptake by 3T3-L1 adipocytes were investigated. The results show that the extract improved the activity of NIT-1 cells damaged by STZ, inhibited glucose absorption into intestinal brush border membrane vesicles and reduced the activity of α-glucosidase. However, gluconeogenesis in H4IIE cells and glucose uptake in 3T3-L1 adipocytes did not change significantly in the presence of the extract. These results suggest that the hypoglycemic mechanisms of the polysaccharide-rich extract of Radix Ophiopogonis are caused by protection in pancreatic islet cells and the inhibition of carbohydrate digestion and absorption. This is possibly the first report on the underlying mechanisms responsible for the antidiabetic effect of Radix Ophiopogonis.

摘要

为了研究麦冬多糖提取物的降血糖机制,研究了该提取物对链脲佐菌素(STZ)损伤的 NIT-1 胰岛素瘤细胞活性、α-葡萄糖苷酶活性、葡萄糖在肠刷状缘膜囊泡中的吸收、H4IIE 肝癌细胞的糖异生和 3T3-L1 脂肪细胞的葡萄糖摄取的影响。结果表明,提取物改善了 STZ 损伤的 NIT-1 细胞的活性,抑制了葡萄糖在肠刷状缘膜囊泡中的吸收,并降低了α-葡萄糖苷酶的活性。然而,提取物存在时,H4IIE 细胞中的糖异生和 3T3-L1 脂肪细胞中的葡萄糖摄取没有明显变化。这些结果表明,麦冬多糖提取物的降血糖机制是通过对胰岛细胞的保护以及对碳水化合物消化和吸收的抑制而产生的。这可能是首次报道麦冬降血糖作用的潜在机制。

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