Stellate Cell Activation and Imbalanced Expression of TGF-β1TGF-β3 in Acute Autoimmune Liver Lesions Induced by ConA in Mice

Abstract EN

Objective.

To study the pathogenic feature of liver injury, activation of hepatic stellate cells, and dynamic expression of TGF-β1/TGF-β3 to reveal their role in liver injury induced by ConA.

Methods.

Mice were randomly divided into control group and ConA treatment group.

ConA (20 mg/kg) was injected through vena caudalis in ConA treatment group; the controls received the same volume of saline injection.

After injection for 2 h, 8 h, 24 h, and 48 h, animals were terminated.

Blood, liver, and spleen were harvested.

Liver function and histopathology were studied.

α-SMA, vimentin, TGF-β1, and TGF-β3 were detected.

Results.

After ConA injection, liver damage started to increase.

Expression of α-SMA, vimentin, TGF-β1, and TGF-β3 was significantly enhanced; all above indicators reached peak at 8 h; but from 24 h after ConA injection, TGF-β3 expression began to decline, while the TGF-β1/TGF-β3 ratio at 48 h was significantly lower than control.

Conclusion.

(1) Autoimmune liver injury induced by ConA showed time-based features, in which the most serious liver lesions happened at 8 h after ConA injection.

(2) Early activation of HSC and imbalance expression of TGF-β1 and TGF-β3 existed in ConA-induced acute autoimmune liver injury, which may be associated with liver dysfunction and the mechanisms of progression to fibrosis.