The Effects of Betulinic Acid on the Expression of Cytokines and Apoptosis-related Proteins in Immune Liver Injury Induced by Concanavalin A
To study the effects of betulinic acid (BA) on the expression of cytokines and apoptosis-related proteins in acute immune liver injury induced by concanavalin A (Con A). Methods
A total of 60 male KM mice were divided into six groups randomly, including control group, Con A model group, bifendate (BIF) group and three BA groups with gradient concentrations. Saline diluted BA (30 mg·kg-1
, 15 mg·kg-1
, 7.5 mg·kg-1
) was given orally to mice. After 15 days' BA pretreatment, mice were then injected with Con A (20 mg·kg-1
) to establish the mouse model with acute immune liver injury. Automatic biochemical analyzer was conducted to determine serum liver function indices such as plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST);ELISA was used to determine the levels of serum inflammatory cytokines (IL-2, IL-4, IL-10, TNF-α, IFN-γ); Western blot was used to detect the expression of liver tissue apoptosis related proteins (Bcl-2 and activated-Caspase-3). Results
Compared with the control group, Con A treated mice showed significantly lower serum ALT and AST levels, while the levels of inflammatory cytokines (IL-2, IL-4, IL-10, TNF-α, IFN-γ) increased significantly. The expression of Bcl-2 was significantly decreased (P
<0.05), whereas the expression of activated-Caspase-3 was significantly increased (P
<0.01). Compared with the Con A model group, the mice that treated with different doses of BA, especially the middle and high dose groups, showed significantly reduced serum ALT and AST levels, as well as significantly decreased serum IL-2, IL-4, TNF-α and IFN-γ levels but increased IL-10. The apoptosis related proteins Bcl-2 and activated-Caspase-3 also showed contrary expression changes: the former increased while the latter decreased. Conclusion
These findings suggested that BA had antagonistic action on the mouse with acute immune liver injury induced by Con A to some extent, and the mechanism of this process may be related with the anti-apoptosis and anti-inflammatory functions of BA to reduce the toxic effects of T lymphocytes.
2016,35(4): 511-516 收稿日期：2016-04-18
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