5092-01-3Relevant articles and documents
Preparation method of 18 beta-methyl glycyrrhetinate
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Paragraph 0024; 0030-0063, (2021/11/27)
The invention provides a preparation method of 18 beta-methyl glycyrrhetinate, which comprises the following steps: taking 18 beta-glycyrrhetinic acid and trimethylsilyl diazomethane as raw materials, and reacting to prepare the 18 beta-methyl glycyrrhetinate. According to the invention, 18 beta-glycyrrhetinic acid is used as a starting material and is subjected to one-step methyl esterification reaction with trimethylsilyl diazomethane to obtain 18 beta-methyl glycyrrhetinate, the synthesis process is simple, the synthesis process conditions are mild, the yield is up to 99.2% or above, the product quality is good, and the content is greater than 99.5%. Besides, through selection of a plurality of parameters such as the solvent, the reaction time and the material dosage, the yield and the purity of the reaction are further improved, and a basis is provided for industrial production.
Synthesis and inhibition of α-glucosidase of methyl glycyrrhetinate glycosides
Zhang, Wei,Wang, He-Ying,Wang, Huai-Xu,Zhu, Zhen-Yuan
supporting information, p. 1874 - 1880 (2019/07/22)
The synthesis of the methyl glycyrrhetinate glycosides and inhibition of α-glucosidase were studied. The carboxyl group of glycyrrhetinic acid was methylated, and glucose and galactose were introduced into the hydroxyl group to obtain compounds 7 and 12.
Synthesis and anti-hepaticfibrosis of glycyrrhetinic acid derivatives with inhibiting COX-2
Bai, Zhongjie,He, Dian,Mohammed, Eyad Abdulwhab Hamoud,Wang, Yanni,Wang, Zhen,Zhang, Qiuping,Zhao, Quanyi
, (2020/04/08)
Many tests have shown cyclooxygenase-2 (COX-2) was closely related to the activation of hepatic stellate cells (HSCs), which further promoting the onset and development of hepatic fibrosis. According to these research findings, a series of glycyrrhetinic acid derivatives were designed and synthesized. Meanwhile, their anti-hepaticfibrotic activities were evaluated in vitro and in vivo. Firstly, in the tests of the cell models, all the compounds displayed anti-proliferative effect on the HSC-T6 activated by (transforming growth factor beta) TGF-β1 (10 ng/mL). Among them, compounds 2 and 16 exhibited a stronger activity than the others, and their IC50 values were 17.6 μM and 30.3 μM, respectively; both of them were low toxicity to normal HSC-T6 cells and WI38 cells, and they inhibited the activated HSC-T6 cells proliferation by promoting apoptosis and resting them at the G0/G1 phase. Secondly, compounds 2 and 16 displayed strong inhibitory effect on activation of HSCs; they not only inhibited the expression of α-SMA and Col1 in the activated HSC-T6 cells, but also decreased the levels of COX-2, TGF-β1 and (reactive oxygen species) ROS in a concentration-dependent manner; they down-regulated the levels of three biomarkers in the process of test, but this decrease did not change linearly with the action time of compound. Thirdly, for the rats which induced with (carbon tetrachloride) CCl4, the symptoms of liver fibrosis in rats were significantly alleviated after successive administration the tested compound for 14d; the α-SMA level in liver tissue decreased in a concentration dependent manner; and the liver cell necrosis and the fat collagen fiber decreased significantly compared with the positive control group; furthermore, inflammatory infiltration was significantly lower than that of the control. This suggests the compounds possibly are candidates for hepatic fibrosis with promising application in clinic.
