RESUMO
PURPOSE: The efficiency of ischemic postconditioning (IPC) was evaluated in a rat model of ischemic liver. Concentration of survivin of liver tissue correlated with the degree of antiapoptosis, so survivin was estimated to evaluate the efficiency of IPC on ischemic reperfusion (IR) injury. METHODS: Twenty-four healthy rats were divided to three groups (SHAM, IR, and IPC). Rats in the SHAM group displayed no change during 3 hours. Rats in the IR group were ischemic within 1 hour of clamping the left hepatic artery and left portal vein. Reperfusion for 2 hours was then done. IPC group, intermittent 2, 3, 5, and 7 minutes of reperfusion followed by 1 hour of warm ischemia. Two-minute reocclusion was done after each reperfusion. Rat sera were analyzed for AST and ALT, and Western blot analysis of rat liver tissue of rats evaluated malondialdehyde (MDA) and survivin. RESULTS: MDA in the liver tissue of rats in the IR and IPC group were significantly high than in the liver tissue of the SHAM group (P = 0.003 and P = 0.008, respectively). Survivin was higher in the IPC group than in the SHAM and IR groups (P = 0.021 and P = 0.024, respectively). CONCLUSION: IPC could not prevent lipid oxidation in liver cell mitochondria, but did aid in the regeneration of ischemic injured liver cells. The results indicate that IPC can suppress the apoptosis of liver cells and reduce reperfusion injury of liver tissue.
RESUMO
PURPOSE: THE AIMS OF THIS STUDY WERE AS FOLLOW: 1) to de scribe the expression status of estrogen receptor-α and -ß mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of 17ß-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. MATERIALS AND METHODS: Detection of estrogen receptor-α and estrogen receptor-ß mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of 17ß-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with 17ß-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. RESULTS: Estrogen receptor-α and estrogen receptor-ß mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, 17ß-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-α nor estrogen receptor-ß antagonist blocked the anti-proliferative effect of 17ß-estradiol. CONCLUSIONS: Our results indicate that estrogen receptor-ß mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-ß positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.
RESUMO
Many studies which focus on the molecules and mechanisms related to the characteristics of the cancer have been performed. In particular, cell adhesion molecules (CAMs) are known to play a central role in the adhesion of cancer cells to vascular endothelial cells. In this study, the expression of CAMs in hepatocellular carcinoma (HCC) cell lines was analyzed and correlated with the characteristics of various HCC cell lines. Eight human HCC cell lines were used in this study. We analyzed the expression of ICAM-1, E-selectin and the integrin subunits of HCC cell lines by western blot analysis and ELISA kit. We estimated the expression of integrin-α5 using western blot analysis and RT-PCR to compare the expression at the gene level with the protein level. In addition, we determined the expression of TGF-ß1, as one of the markers for the cellular activity compared to the levels of expression with the expression of integrin-α3 and -α5. ICAM-1 was highly expressed in all of the cell lines except SNU398 and Hep3B, which exhibit a more aggressive nature among the studied HCC cell lines. E-selectin and integrin subunits varied in all HCC cell lines. In particular, integrin-ß2 was highly expressed on all HCC cell lines. In conclusion, the levels of expression of the CAMs may not affect cellular activity, morphology or tumorigenicity. However, most HCC cell lines show various expressions of CAMs, suggesting that HCC cell lines expressing the major CAMs remain candidates for molecular targeted therapy, which may need to be patient-tailored for therapy according to the molecular profile.
