The plasma levels of transforming growth factor beta1 and the protein expressions of alpha-SMA, urokinase plasminogen activator and plasminogen activator inhibitor-1 in liver of patients with different grades of hepatic fibrosis.
- Author:
Xi-Run WU
1
;
Min-He LV
;
Qi WANG
;
Shui-Sheng SHI
;
Wen-Dong GUO
Author Information
- Publication Type:Journal Article
- MeSH: Actins; blood; Adult; Aged; Female; Hepatitis B, Chronic; blood; complications; Humans; Liver Cirrhosis; blood; etiology; Male; Middle Aged; Plasminogen Activator Inhibitor 1; blood; Transforming Growth Factor beta; blood; Transforming Growth Factor beta1; Urokinase-Type Plasminogen Activator; blood
- From: Chinese Journal of Hepatology 2004;12(7):400-402
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo measure the plasma levels of transforming growth factor beta1 (TGFbeta1), the protein expression of alpha-SMA in hepatic stellate cells and urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1), and study on the relationships between the plasma levels of TGFbeta1, the protein expression and the serum hyaluronic acid (HA) in patients with different grades of hepatic fibrosis.
METHODSThirty seven cases with hepatic fibrosis of different grades were classified according to HE and VG staining categories from 0 to 4, in which there were 8 cases in grade 1, 9 cases in grade 2, 7 cases in grade 3, 13 cases in grade 4. The plasma levels of TGFbeta1 and the serum levels of HA were detected by ELISA. The protein expressions of a-SMA, uPA and PAI-1 in fibrotic liver tissue were observed by immunohistochemistry.
RESULTSWith the progression of hepatic fibrosis, the plasma levels of TGFbeta1 and the protein expression of a-SMA, uPA and PAI-1 in fibrotic liver tissue were increased. In grade 3 and 4, the plasma levels of TGFbeta and the protein expression of a-SMA and PAI-1 in fibrotic liver tissue were significantly increased, but the protein expression of uPA in cirrhosis liver tissue did not increased.
CONCLUSIONTGFbeta1, a-SMA, uPA and PAI-1 play an important role in the progression of hepatic fibrosis. Inhibiting the early activation of latent TGFbeta1 or increasing uPA and inhibiting PAI-1 over express may contribute to matrix degradation and retard the progression of hepatic fibrosis.