ArticleZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology2016
[Role of glycogen synthase kinase-3β in development of severe hepatitis liver failure caused by hepatitis B virus].
Article in Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- [Protective effect of glycogen synthase kinase 3β inhibition via peroxisome proliferator-activated receptor alpha activation in mice with acute liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017Article
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11 authors at 2 institutions in 1 country.
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Abstract
objectiveTo investigate the role of glycogen synthase kinase-3β (GSK3β) in the development of severe hepatitis liver failure (SHLF) caused by the hepatitis B virus.
methodsTwelve patients with chronic hepatitis B (CHB) (CHB group), 12 patients with SHLF caused by hepatitis B virus (SHLF group), and 8 normal subjects (control group), who were admitted to Beijing You'an Hospital from January 2009 to December 2011, were included in this study. Their liver tissues were collected to do some clinical examinations. The GSK3β activity in the liver tissue was detected with a GSK3β activity assay kit. Western blot was used to determine the expression of p-GSK3, total GSK3, and -actin. The paraffin sections of liver tissue were prepared for immunofluorescence assay. All data were expressed as mean±standard deviation, and comparison between groups was made by least significant difference t test. P < 0.05 was considered statistically significant.
resultsWestern blot results showed that compared with the control group, the CHB group had a higher level of p-GSK3β and the SHLF group had a significantly lower level of p-GSK3β (P = 0.0342). The immunofluorescence assay results showed that the SHLF group had a significantly lower level of p-GSK3β than the control group. GSK3β activity assay results showed that compared with the control group, the CHB group had a significantly lower GSK3β activity and the SHLF group had a significantly higher GSK3β activity (P = 0.0289), which were consistent with the results of Western blot and immunofluorescence assay.
conclusionGSK3 is activated in the development of SHLF, so it is an important signaling molecule in the pathogenesis of SHLF. Inhibiting its activity may play a role in the prevention and treatment of SHLF.
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