Influences of vitamin E on the expression of tissue inhibitor of metalloproteinase-2, type III collagen and fibronectin in CCL_4-induced rats liver fibrosis.
Yuming Wang
Abstract
Yuming Wang
Abstract
Objective To study the influences of vitamin E(VE) on liver fibrosis and its mechanism of action. Methods Liver fibrosis was induced in rats by the administration of CCL 4. The treatment group was treated with VE(100 mg/kg, IV) twice a week for 10 weeks after the liver fibrosis model was established. Immunohistochemical staining of hepatic type Ⅲ collagen protein and fibronectin were carried out in the 10th week after the administration of VE. At the same time, the hepatic contents of α 1(Ⅲ) procollagen and tissue inhibitor of metalloproteinase 2(TIMP 2)mRNA were observed with in situ hybridiznion. Results There were much less type Ⅲ collagen protein and fibronectin in the liver in the group treated with VE than that in the control. The expression of TIMP 2 and α 1(Ⅲ) procollagen mRNA were significantly inhibited in the treatment group. These changes were statistically significant as compared with that of the control group as examined by an image analysis system( P 0.05)。 Conclusion VE treatment can down modulate the expression of TIMP 2 mRNA in rats with liver fibrosis, thereby, play a role in the attenuation of fibrosis.
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Objective To study the influences of vitamin E(VE) on liver fibrosis and its mechanism of action. Methods Liver fibrosis was induced in rats by the administration of CCL 4. The treatment group was treated with VE(100 mg/kg, IV) twice a week for 10 weeks after the liver fibrosis model was established. Immunohistochemical staining of hepatic type Ⅲ collagen protein and fibronectin were carried out in the 10th week after the administration of VE. At the same time, the hepatic contents of α 1(Ⅲ) procollagen and tissue inhibitor of metalloproteinase 2(TIMP 2)mRNA were observed with in situ hybridiznion. Results There were much less type Ⅲ collagen protein and fibronectin in the liver in the group treated with VE than that in the control. The expression of TIMP 2 and α 1(Ⅲ) procollagen mRNA were significantly inhibited in the treatment group. These changes were statistically significant as compared with that of the control group as examined by an image analysis system( P 0.05)。 Conclusion VE treatment can down modulate the expression of TIMP 2 mRNA in rats with liver fibrosis, thereby, play a role in the attenuation of fibrosis.
Key concepts: Procollagen peptidase, Fibronectin, Fibrosis, Immunohistochemistry, Hydroxyproline, Internal medicine, Tissue inhibitor of metalloproteinase, Endocrinology