Therapeutic effects of velvet antler polypeptides on hepatic fibrosis in rats

来源 :中国药理学与毒理学杂志 | 被引量 : 0次 | 上传用户:heatsink
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OBJECTIVE To explore the therapeutic effects and underlying mechanisms of velvet antler polypeptides(VVAPs)in CCl4-induced experimental hepatic fibrosis in rats.METHODS Anti-hepatic fibrosis properties of VAPs were tested by Subcutaneous injection(SC)into male Wistar rats of CCl4- induced experimental hepatic fibrosis.After SC injections for 45 consecutive days at doses of 5mg·kg-1(low dose,VAPsL),10mg·kg-1(mid-dose,VAPsM)and 20mg·kg-1(high-dose,VAPsH),the rats were sacrificed and the various indicators were evaluated and tested.Observed hepatic cells degeneration and necrosis,inflammatory infiltration and levels of serum enzymes to assess treatment of VAPs;The expression levels of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),MDA,and hydroxyproline(HYP)in liver tissue were analyzed;RT-PCR analysis was carried out to detect the expression levels of matrix metalloproteinases2(MMP-2)and tissue inhibitor of metalloproteinases 1(TIMP-1)in liver tissue.RESULTS VAPs has obvious anti-hepatic fibrosis effects.Hepatocyte swelling,fatty degeneration was significantly reduced,reducing infiltration of inflammatory cells.Release of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)decreased significantly,reduction of hyaluronic acid(HA)and laminin(LN)obviously,at the same time,the content of total protein and albumin increased significantly in serum.Activity of SOD and GSH-Px was significantly raised and the content of MDA and HYP was reduced significantly in liver tissue.Expression levels of MMP-2and TIMP-1 mRNA in liver were decreased significantly.These improvements were more significant in high-dos and mid-dose groups(P<0.05 or P<0.01 vs model group).CONCLUSION These findings suggest VAPs can significant treat the hepatic fibrosis,which may be due to protect liver cells and improve liver functions by hydroxyl radical scavenging activity and great effect of antioxidation,and decrease the gene expression of MMP-2,improving exist-environment of liver cells and decreasing the gene expression of TIMP-1,prompting degradation of extracellular matrix. OBJECTIVE To explore the therapeutic effects and underlying mechanisms of velvet antler polypeptides (VVAPs) in CCl4-induced experimental hepatic fibrosis in rats. METHODS Anti-hepatic fibrosis properties of VAPs were tested by Subcutaneous injection (SC) into male Wistar rats of CCl4-induced experimental hepatic fibrosis. After SC injections for 45 consecutive days at doses of 5 mg · kg -1 (low dose, VAPsL), 10 mg · kg -1 (mid-dose, VAPsM) and 20 mg · kg -1 ), the rats were sacrificed and the various indicators were evaluated and tested. Observed hepatic cells degeneration and necrosis, inflammatory infiltration and levels of serum enzymes to assess treatment of VAPs; The expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH- Px), MDA, and hydroxyproline (HYP) in liver tissue were analyzed; RT-PCR analysis was carried out to detect the expression levels of matrix metalloproteinases 2 (MMP-2) and tissue inhibitor of metalloproteinases 1 (TIMP- .RESULTS VAPs has obvious reducing of hyaluronic acid (HA) and laminin (LN) obviously. Hepatitis B virus (ALT) and aspartate aminotransferase , at the same time, the content of total protein and albumin increased significantly in serum. Activity of SOD and GSH-Px was significantly raised and the content of MDA and HYP was reduced significantly in liver tissue. Expression levels of MMP-2 and TIMP- 1 mRNA in liver were decreased significantly. These improvements were more significant in high-dos and mid-dose groups (P <0.05 or P <0.01 vs. model group.) CONCLUSION These findings suggest VAPs can be significant for the hepatic fibrosis, which may be due to protect liver cells and improve liver functions by hydroxyl radical scavenging activity and great effect of antioxidation, and decrease the gene expression of MMP-2, improving exist-environment of liver cells and decreasing the gene expression of TIMP-1, prompting degradation of extracellular matrix.
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