Search

为合理开发利用买麻藤种仁，以云南省垂子买麻藤种仁和小叶买麻藤种仁为研究对象，对其形态指标和营养品质指标进行分析及评价，并对基本营养成分、氨基酸、脂肪酸、矿物质元素等60项营养品质指标进行相关性分析。结果表明：垂子买麻藤种仁的长、宽、长宽比、千粒重形态指标均较大，分别是小叶买麻藤种仁的1.78、1.58、1.12倍和4.15倍；垂子买麻藤种仁的粗蛋白质（13.53%）、可溶性糖（6.25%）、总黄酮（1.09%）、γ-氨基丁酸（1.98 mg/g）、Ca（607.30 mg/kg）、Mn（46.44 mg/kg）、Ni（5.48 mg/kg）含量和硬脂酸（25.42%）、α-亚麻酸（1.49%）、γ-亚麻酸（2.63%）相对含量均极显著高于小叶买麻藤种仁的（p＜0.01），小叶买麻藤种仁的干物质（59.56%）、淀粉（53.49%）、粗脂肪（2.48%）、粗纤维（2.50%）、P（2 812.73 mg/kg）、Mg（1 619.95 mg/kg）、Na（8.41 mg/kg）、Zn（11.87 mg/kg）、Sr(2.26 mg/kg)、亮氨酸（15.13 mg/g）等10种氨基酸含量和花生酸（1.78%）、油酸（17.41%）相对含量均极显著高于垂子买麻藤种仁的（p＜0.01）；相关性分析结果显示，有约40%的营养品质指标间具有极强的相关性。综上，两种买麻藤种仁在形态指标和营养品质指标中均存在明显差异，具有不同的营养特征。In order to develop and utilize the Gnetum seed kernel rationally, the morphology and nutritional quality indexes of seed kernels of Gnetum pendulum and Gnetum parvifolium from Yunnan province were analyzed and evaluated, and the correlation of 60 nutritional quality indexes including basic nutritional components, amino acids, fatty acids and mineral elements were analyzed. The results showed that the length, width, ratio of length to width and 1 000-grain weight of Gnetum pendulum seed kernel were higher, which were 1.78, 1.58, 1.12 times and 4.15 times as many as Gnetum parvifolium seed kernel. The contents of crude protein (13.53%), soluble sugar (6.25%), total flavone (1.09%), γ-aminobutyric acid (1.98 mg/g), Ca (607.30 mg/kg), Mn (46.44 mg/kg), Ni (5.48 mg/kg) and the relative content of stearic acid (25.42%), α-linolenic acid (1.49%), γ-linolenic acid (2.63%) of Gnetum pendulum seed kernel were significantly higher than those of Gnetum parvifolium seed kernel (p

Copyright of Acta Agronomica Sinica is the property of Crop Science Society of China and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Medicine & Health is the property of Journal of Modern Medicine & Health and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of carrimycin on the biological function of pancreatic cancer cells. Methods Pancreatic cancer cell lines MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 were treated with carrimycin at concentrations of 0 (control group), 2, 4, 8, and 16 μmol/L for 24, 48, and 72 hours. MTT assay was used to measure cell viability; EdU cell proliferation assay was used to observe the effect of carrimycin on DNA replication of pancreatic cancer cells; colony formation assay was used to observe the effect of carrimycin on the proliferation of pancreatic cancer cells; flow cytometry was used to analyze the effect of carrimycin on the cell cycle of pancreatic cancer cells; wound healing assay was used to analyze the effect of carrimycin on the migration of pancreatic cancer cells; Western blot was used to measure the expression levels of the markers such as epithelial-mesenchymal transition (EMT) and cell cycle-dependent protein kinase inhibitor 1 A (P21); immunofluorescence assay were used to measure the expression levels of EMT-related markers. An analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results Compared with the control group, carrimycin significantly inhibited the proliferative activity of MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 cells in a concentration-and time-dependent manner (all P<0.01); carrimycin at concentrations of 4, 8, and 16 μmol/L significantly reduced DNA replication in MIA PaCa-2 cells (t=2.378, 4.984, and 18.970, all P<0.05) and BxPC-3 cells (t=4.879, 6.089, and 9.521, all P<0.01); after treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, colony formation ability significantly decreased with the increase in drug concentration in MIA PaCa-2 cells (t=5.889, 11.240, and 15.840, all P<0.001) and BxPC-3 cells (t=6.717, 15.800, and 18.850, all P<0.001). After treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, there was a significant increase in the proportion of cells in G1 phase in MIA PaCa-2 cells (t=9.071, 12.280, and 19.360, all P<0.0001) and BxPC-3 cells (t=3.061, 4.962, and 8.868, all P<0.05), and there was a significant reduction in the proportion of cells in S phase in MIA PaCa-2 cells (t=2.316, 4.165, and 5.562, all P<0.05) and BxPC-3 cells (t=2.424, 3.264, and 5.744, all P<0.05). Western blot further demonstrated that compared with the control group, the expression level of the cell cycle-related protein P21 gradually increased with the increase in the concentration of carrimycin in MIA PaCa-2 cells (t=5.437, 6.453, and 8.799, all P<0.001) and BxPC-3 cells (t=25.130, 44.750, and 52.960, all P<0.000 1). Wound healing assay showed that after treatment for 12, 24, and 48 hours, carrimycin at concentrations of 0, 4, 8, and 16 μmol/L significantly reduced the lateral migration of MIA PaCa-2 cells (all P<0.05) and BxPC-3 cells (all P<0.05). Western blot showed that compared with the control group, carrimycin treatment at concentrations of 4, 8, and 16 μmol/L significantly upregulated the expression of the epithelial marker E-cadherin in MIA PaCa-2 cells (t=2.388, 4.899, and 5.819, all P<0.05) and BxPC-3 cells (t=2.533, 5.836, and 6.774, all P<0.05) and significantly downregulated the expression of the interstitial marker Snail in MIA PaCa-2 cells (t=12.440, 14.830, and 16.800, all P<0.000 1) and BxPC-3 cells (t=5.039, 5.893, and 7.725, all P<0.01), and it also significantly downregulated the expression of the interstitial marker Vimentin in MIA PaCa-2 cells (t=3.105, 7.752, and 11.200, all P<0.05) and BxPC-3 cells (t=2.555, 4.883, and 9.153, all P<0.05). Conclusion Carrimycin can effectively inhibit the proliferation, migration, and EMT process of pancreatic cancer cells, thereby exerting an antitumor biological activity. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Ecology & Rural Environment is the property of Journal of Ecology & Rural Environment Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)