首页> 美国卫生研究院文献>Molecules >Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl4-Induced Chronic Hepatotoxicity in Mice
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Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl4-Induced Chronic Hepatotoxicity in Mice

机译:人参皂苷原人参皂苷制备人参皂苷M1的Snailase及其对CCl4诱导的小鼠慢性肝毒性的保护作用

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摘要

To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl4)-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The optimum time for the conversion was 24 h at a constant pH of 4.5 and an optimum temperature of 50 °C. The transformation products were identified by high-performance liquid chromatography and electrospray ion-mass spectrometry. Subsequently, most of PDG was decomposed and converted into G-M1 by 24 h post-reaction. During the study on hepatoprotective in a mice model of chronic liver injury, PDG or G-M1 supplement significantly ameliorated the CCl4-induced liver lesions, lowered the serum levels of select hepatic enzyme markers (alanine aminotransferase, ALT, and aspartate aminotransferase, AST) and malondialdehyde and increased the activity of superoxide dismutase in liver. Histopathology of the liver tissues showed that PDG and G-M1 attenuated the hepatocellular necrosis and led to reduction of inflammatory cell infiltration. Therefore, the results of this study show that PDG and G-M1 can be proposed to protect the liver against CCl4-induced oxidative injury in mice, and the hepatoprotective effect might be attributed to amelioration of oxidative stress.
机译:为了研究原人参二醇型人参皂苷(PDG)及其代谢产物人参皂苷M1(G-M1)对四氯化碳(CCl4)诱导的ICR小鼠慢性肝损伤的保护作用,我们进行了原人参二醇型人参皂苷向人参皂苷M1的转化。使用蜗牛酶。在4.5的恒定pH和50°C的最佳温度下,转化的最佳时间为24小时。通过高效液相色谱和电喷雾离子质谱法鉴定转化产物。随后,大多数PDG分解,并在反应后24小时转化为G-M1。在对慢性肝损伤小鼠模型进行保肝研究期间,PDG或G-M1补充剂可显着改善CCl4诱导的肝损伤,降低血清中某些肝酶标记物(丙氨酸氨基转移酶,ALT和天冬氨酸氨基转移酶AST)的水平。和丙二醛,增加肝脏超氧化物歧化酶的活性。肝组织的组织病理学研究表明,PDG和G-M1减弱了肝细胞坏死并导致炎性细胞浸润减少。因此,这项研究的结果表明,PDG和G-M1可以被提议保护肝脏免受CCl4诱导的小鼠氧化损伤,并且其肝保护作用可能归因于氧化应激的减轻。

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