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首页> 外文期刊>Archives of histology and cytology. >The inhibition of apoptosis by glycyrrhizin in hepatic injury induced by injection of lipopolysaccharide / D-galactosamine in mice.
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The inhibition of apoptosis by glycyrrhizin in hepatic injury induced by injection of lipopolysaccharide / D-galactosamine in mice.

机译:甘草甜素对小鼠注射脂多糖/ D-半乳糖胺所致肝损伤的凋亡抑制作用。

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摘要

The inhibition of apoptosis by glycyrrhizin (GL) in hepatic injury induced by injection of lipopolysaccharide (LPS)/D-galactosamine (D-GalN) was examined in the present study. Morphological and biochemical analyses of LPS/D-GalN-induced mouse liver injury revealed that apoptosis occurred exclusively in injured hepatocytes of the centrilobular area. The degree of hepatic injury was associated with a substantial number of hepatocytes undergoing apoptosis. Transaminase levels were significantly increased at 6 to 8 h after the injection of LPS/D-GalN compared with controls. GL inhibited the elevation of serum transaminase levels when it was given to mice at 30 min before the administration of LPS/D-GalN. Morphological analyses using the TUNEL-method showed GL significantly reduced the number of TUNEL-labeled cells in acute hepatitis induced with LPS/D-GalN-treatment. Cells from the pericentral hepatic injury region were dissected out using a microdissection-method, and the DNA-ladder was clearly documented. Furthermore, results obtained through the TUNEL-method were confirmed with an oligonucleosome-bound DNA ELISA. From the current results, it seems reasonable to conclude that the protective role of GL in LPS/D-GalN-induced liver injury is performed through the inhibition of hepatic apoptosis.
机译:在本研究中,研究了甘草甜素(GL)在注射脂多糖(LPS)/ D-半乳糖胺(D-GalN)诱导的肝损伤中对细胞凋亡的抑制作用。 LPS / D-GalN引起的小鼠肝损伤的形态学和生化分析表明,凋亡仅发生在受损的小叶区肝细胞中。肝损伤的程度与大量经历凋亡的肝细胞有关。与对照组相比,注射LPS / D-GalN后6至8小时,转氨酶水平显着增加。当在LPS / D-GalN给药前30分钟给予小鼠时,GL抑制了血清转氨酶水平的升高。使用TUNEL方法进行的形态学分析表明,GL显着减少了LPS / D-GalN治疗诱导的急性肝炎中TUNEL标记的细胞数量。使用显微解剖方法将中心肝周围损伤区域的细胞解剖出来,清楚地记录了DNA梯子。此外,通过TUNEL法获得的结果用寡核苷酸结合的DNA ELISA证实。从目前的结果来看,似乎合理的结论是,GL在LPS / D-GalN诱导的肝损伤中的保护作用是通过抑制肝细胞凋亡来实现的。

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