Mechanism of oxymatrine in preventing hepatic fibrosis formation in patients with chronic hepatitis B.
- Author:
Jian-xin LIANG
1
;
Xing-fen QU
;
Wen-ting ZENG
;
Ke-lun ZHU
;
He ZHANG
;
Jian-jun WEI
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Alkaloids; therapeutic use; Female; Hepatitis B, Chronic; drug therapy; pathology; Humans; Interleukin-10; blood; Liver Cirrhosis; drug therapy; pathology; prevention & control; Male; Middle Aged; Quinolizines; therapeutic use; Transforming Growth Factor beta1; blood; Tumor Necrosis Factor-alpha; blood
- From: Journal of Southern Medical University 2010;30(8):1871-1873
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the mechanism of oxymatrine in preventing hepatic fibrosis formation in patients with chronic hepatitis B (CHB).
METHODSA total of 80 CHB patients receiving routine therapies for liver protection and support were divided into two groups. Oxymatrine at the daily dose of 150 mg was injected intravenously in the therapeutic group (n=40), and gluthion (1.2 g daily) was injected in the control group (n=40) for 8 weeks. The liver functions, indexes of hepatic fibrosis and the levels of transforming growth factor-beta1 (TGF-beta1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) were measured in these patients before and after the therapy.
RESULTSLiver functions was obviously improved after therapy in both groups, showing no significant difference between them (P>0.05). The indexes of hepatic fibrosis such as HA, LN, PCIII and C-IV were significantly lower in the therapeutic group than in the control group (P<0.01). The serum levels of TGF-beta1 and TNF-alpha decreased while IL-10 increased significantly after the treatment in the therapeutic group (P<0.05).
CONCLUSIONThe effect of oxymatrine against hepatic fibrosis is mediated by lowering the levels of TGF-beta1 and TNF-alpha and increasing the level of IL-10 in CHB patients.
