Journal of Southern Medical University ›› 2014, Vol. 34 ›› Issue (02): 201-.
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Abstract: Objective To investigate the changes in the functional activity of glycogen synthase kinase-3 (GSK-3) in the hepatictissue after endotoxin (lipopolysaccharide, LPS) tolerance and explore the effects of LPS-induced GSK-3 inhibition on glycogenmetabolism in the liver. Methods Male SD rats were randomly divided into normal control, endotoxin pretreatment andGSK-3 inhibitor (lithium chloride) groups with corresponding pretreatments prior to a large dose of LPS challenge (10 mg/kg)to induce liver injury. Glycogen deposition and content in the hepatic tissue was detected using periodic acid-Schiff (PAS)staining and a glycogen quantification kit, respectively. Western blotting was performed for semi-quantitative analysis ofprotein level and inhibitory phosphorylation of GSK-3, and a Coomassie brilliant blue G-250-based colorimetric assay wasused to detect calpain activity in the liver. Results Glycogen content in the liver decreased significantly after LPS challenge inall the 3 groups (P<0.05) but showed no significant difference among the groups (P>0.05). Both LPS and lithium chloridepretreatments caused a significant increase of liver glycogen content (P<0.05). LPS pretreatment induced inhibitoryphosphorylation of GSK-3β (P<0.05) and partial cleavage of GSK-3α but did not affect the expression of GSK-3 protein (P>0.05). Large-dose LPS challenge significantly increased the activity of calpain in the liver tissue (P<0.05) to a comparable levelin the 3 groups (P>0.05). Conclusion Endotoxin pretreatment induces inhibitory phosphorylation of GSK-3β and partialcleavage of GSK-3α and promotes the deposition of liver glycogen but does not affect the activity of calpain, which maycontribute to an increased glycogen reserve for energy supply in the event of large-dose LPS challenge.
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https://www.j-smu.com/EN/Y2014/V34/I02/201