The Expression of G1 Cycins and Rb-E2F, and the Effect of Vitamin E on Hepatic Stellate Cells Activated by CCl4

Abstract

Background/Aims: It is obscure when the activation of hepatic stellate cells and the expression of its related factors occur in acute liver injury. Vitamin E is expected to prevent hepatic fibrosis. The aims of this study were

to establish the model of hepatic stellate cell activation in acute liver injury and to confirm the effect of vitamin E for preventing hepatic fibrosis. Methods: Male Sprague-Dawley rats were classified into two groups. The

one group received a single injection of CCl4 and the other group received injection of vitamin E daily and a single injection of CCl4. The serial changes of serum ALT, and [3H]thymidine uptake, α-SMA, cyclin D1,

CDK4,

cyclin E, CDK2, Rb, E2F-1 and NF-κB of stellate cells were measured. Results: The

serial changes of serum ALT levels, [3H]thymidine uptake, and α-SMA positive cells showed maximum increase at 32 hours after CCl4 injection. However, they were significantly decreased with injection of vitamin E. CDK4,

cyclin

E

and CDK2 showed definite band at 16, 32, 48 hours after CCl4 injection, which

diminished or disappeared with injection of vitamin E. Cyclin D1, Rb, E2F-1 and NF-κB showed definite band at 32 hours after CCl4 injection, which also diminished or disappeared with injection of vitamin E. Conclusions: We

established

an in vivo model of hepatic stellate cell activation in acute liver injury and confirmed the effect of vitamin E in preventing hepatic fibrosis.