| Objective: The hepatocellular carcinoma is one of the clinically common malignant tumors,which has high mortality and difficult to cure. It progresses fast,invade,transfer and recur easily. Along with the development of medical technology and medical research,have already had a great exaltation to the diagnosis and the treatment technique of HCC. But at present the certain mechanism of HCC genesis is not clear,there is no effective protective measure yet. Thus it's greatly significant in clinic to research the etiopathogenesis of HCC and investigate new protective measure.Peroxisome proliferator activated receptor is a new member of the NHR super family. PPARs subfamily has defined as PPARα, PPARβand PPARγ. They differ in their structure, function and tissue distribution specificity. Several lines of evidence indicate that PPARγplays an important role in regulating adipocyte and glucose metabolism,adipocyte differentiation,energy balance,inflammatory reaction,artherosclerosis,inducing differentiation and apoptosis of tumor cell. Recent data showed that ligands for PPARγoverexpressed in many tumor cell, through various paths inhibited tumor cell proliferation,induced apoptosis and differentiation,inhibited angiogenesis and depressed invasion of tumor cell.PPARγcontains natural and synthetical ligands. The former by derivation from the prostaglandin D2 by the experiment confirmation of a series of prostaglandin metabolism is the PPARγof natural ligands,among them 15d-PGJ2 combines strongest to the PPARγ.The synthetical ligands mainly is the thiazolidinediones of euglycemic agent such as rosiglitazone, pioglitazone, troglitazone.This medicine mainly used for theⅡtype the treatment of the diabetes on the clinic. Some experiment of the abroad certificate the PPARγexcitomotory can prevent tumorous development availably,hoping can play an important on tumorous chemical prophylaxis.Rosiglitazone is the drug which is the highest bioavailability and drug action.Our previous experiment indicated rosiglitazone can significantly inhibit the growth of SMMC-7721 cell line .Our experiment further reveal the possible mechanism of action on the inhibition of hepatoma growth by investigating the effect of rosiglitazone(PPARγagent)on the genetic expression of VEGF,AKT1/2 and P-AKT1 of SMMC-7721 cell line.Methods: 1 We detected the protein expression of VEGF by Western Blot in four groups which were administered with rosiglitazone of various concentrations,0.1,1,10,100(μmol/L)respectively and the cell joined 10μmol/L of rosiglitazone,and on three action times(24h,48h,72h)in each group. 2 We determined the protein expression of AKT1/2,P-AKT1 by Western Blot in three groups which were administered with rosiglitazone of various concentrations,1,10,100μmol/L respectively and the cell joined 10μmol/L of rosiglitazone,and on four action times (0.5h,1h,2h,6h) in each group. By analysis of variance for one factors (ANOVA), optical density was analysised to investigate time-effect relationship and quantity-effect relationship.Results:1 Western-blot showed that rosiglitazone can decrease the expression of protein VEGF in human hepatoma cell line SMMC-7721 in a dose-dependence and time-dependent manner( P<0.05).2 Detect the expression of AKT1/2,P-AKT1 by Western Blot: No obvious difference of expression of AKT1/2,P-AKT1were found(P>0.05).Conclusion:1 Rosiglitazone can decrease the expression of protein VEGF in human hepatocellular carcinoma cell line SMMC-7721 in a dose-dependence and time-dependent manner(P<0.05).The result suggested that rosiglitazone can inhibit the angiogenesis,cell proliferation and metastasis of HCC, It is suggested that rosiglitazone may be a potential molecular therapeutic target for Hepatocellular carcinoma.2 The result show that rosiglitazone was not significantly related with the expression of AKT1/2,P-AKT1(P>0.05). It shows that rosiglitazone decreasing the expression of protein VEGF perhaps do not inhibit the PI3K/AKT signal conduction pathway.
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