Abstract

Objective To investigate the changes of helper T cell 17(Th17) and regulatory T cell (Treg) subsets and cytokine levels in peripheral blood of mice with acute liver injury induced by D-galactosamine(D-GalN) and lipopolysaccharide(LPS). Methods Total of 36 specefic pathogen free(SPF) male BALB/c mice were randomly divided into control group and model group.The model group were injected with D-GalN and LPS solution to establish mouse model with acute liver injury, while the control mice were injected with equal volume of saline.Serum aspartate transaminase(AST) and alanine transaminase(ALT) were detected by enzyme linked immunosorbent assay (ELISA). The liver injury of mice was detected by HE staining.Th17 and Treg in peripheral were detected by flow cytometry.Serum interleukin(IL)-17, IL-6, IL-23, tumor necrosis factor-α(TNF-α), IL-10, and transforming growth factor-β(TGF-β)were analyzed with enzyme linked immunosorbent assay(ELISA). Results Compared with control mice, serum AST and ALT of the model mice were significantly increased (t=5.39, 4.92, P<0.05). Pathological staining showed that the liver tissue of model mice was severely damaged, indicating that the mouse model of acute liver injury was successfully generated.Th17 cells in model mice were significantly increased, the Treg cells were significantly decreased, whereas the Th17/Treg cell ratio increased significantly (t values were 3.87, 3.25 and 5.50 respectively, all P values<0.05). IL-17, IL-6, TNF-α, and IL-23 in model mice were significantly increased, while IL-10 and TGF-βwere significantly decreased (t values were 4.33, 5.60, 4.05, 3.68, 3.12 and 3.03 respectively, all P values<0.05). Conclusion Th17/Treg cells and related cytokines in peripheral blood of mice with acute liver injury induced by D-GalN/LPS are seriously imbalanced, which may play an important role in the development of acute liver injury. Key words: D-galactosamine; Lipopolysaccharide; Acute Liver injury; Helper T cell 17; Regulatory T cell; Cytokine

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call