The Study Of Peroxisome Proliferator-activated Receptor-γModulating Vascular Endothelial Growth Factor-D Expression

Objective Detect the expression of peroxisome proliferator-activated receptor-y, vascular endothelial growth factor-D and lymphatic vessel density in gastric cancer to analyze the correlation between the three and clinical pathological factors.Methods The expression of PPAR-y,VEGF-D and LVD which was marked with D2-40were detected by immunohistochemistry in each44cases lymph node metastasis and no lymph node metastasis specimens, the same number of normal stomach tissue using as a control.Results The positive rate of PPAR-y in no lymph node metastasis tissue was86.4%(38cases) which was significantly higher than in lymph node metastasis tissue59.1%(26cases) and normal stomach tissue38.6%(17cases)(P<0.01). The positive rate of VEGF-D was54.5%(24cases),81.8%(36cases) and31.8%(14cases)(P<0.01). Both expression were relevant to differentiation degree and TNM staging (P<0.05).The expression of LVD in PPAR-y positive group was significantly lower than in PPAR-y negative group (P<0.01).The expreession differences of LVD were relevant to TNM staging and lymph node metastasis (P<0.01). PPAR-y was negatively correlated with VEGF-D(r=-0.347, P<0.05) while VEGF-D and LVD was positively correlated(r=0.419, P<0.05).Conclusions PPAR-y, VEGF-D and LVD have high expression in gastric cancer tissue. PPAR-y maybe through suppressing the expression of VEGF-D to reduce the LVD and inhibit the lymph node metastasis. Objective Research the influence and possible mechanism of PPAR-y agonists rosiglitazone, insulin, indomethacin to new lymphatic vessel form in gastric cancer.Methods Cell immunohistochemistry and Western-blot were used to detect the expression of PTEN and VEGF-D in the BGC-823gastric cancer cell lines which had been intervened by rosiglitazone, indomethacin, insulin with different concentrations for48hours.Results Cell immunohistochemistry and Western-blot results showed us the expression of PTEN were dose dependently increased after the cell been intervened by rosiglitazone, indomethacin and insulin with different concentrations for48hours. On the contrary VEGF-D were dose dependently decreased.Conclusion The three agonists can activate the PPAR-y and inhibit the VEGF-D expreession through up-regulating the PTEN gene expression. Objective To investigate the regulation of activated peroxisome proliferator-activated receptor-y on vascular endothelial growth factor-D expression and it’s possible mechanism.Methods Xenograft tumor model were established by inoculating the cell line BGC-823which had been intervened with200,100,50and0μmol/L concentrations of rosiglitazone for48hours into the nude mice subcutaneously. The PTEN and VEGF-D expression were detected by immunohistochemistry in nude mice tumor tissues.Results The expression level of PTEN in200,100and50μmol/L ROS groups were significantly higher than in0μmol/L (P<0.01) according to the cell immunohistochemistry results and nude mice tumor tissues immunohistochemistry results while VEGF-D were significantly lower (P<0.01).Both of the expression differences between the200,100and50μmol/L ROS groups were statistically significant (P<0.05). Rosiglitazone can significantly and dose dependently decrease the nude mice tumor volume and increase the tumor inhibition rates(P<0.01).Conclusion The activated PPAR-y can suppress VEGF-D expression. The mechanism may be related to the up-regulation of PTEN gene expression.