The expressions and significance of Hpa and bFGF in oral squamous-cell carcinoma

Objective： To investigate the expressions of heparanase （Hpa） and basic fibroblast growth factor （bFGF） in oral squamous-cell carcinoma （OSCC）, and to evaluate the relationship between the expressions and tumor angiogenesis and progression. Methods： The expressions of Hpa mRNA and bFGF mRNA of OSCC were examined using in situ hybridization. The microvascular density （MVD） was assessed through immunohistochemistry staining. Results： The expressions of Hpa mRNA and bFGF mRNA were associated with tumor MVD and lymph node metastasis. Concomitant expression of Hpa mRNA and bFGF mRNA was associated with higher tumor MVD as compared with expression of either factor alone. Conclusion： Hpa and bFGF might contribute to the angiogenesis and lymph node metastasis in OSCC and they cooperate in promoting vascularization.

CORRELATIONS AMONG EXPRESSION OF ANGIOPOIETIN-1 TO CLINICAL PATHOLOGICAL CHARACTERISTICS AN ANGIO-GENESIS IN ORAL SQUAMOUS CELL CARCINOMA

Objective： To study the expression and the significance of Angiopoietin-1 （Ang-1） through observing the correlations among the expression of Ang-1 to clinicopathologic characteristics and microvessel density （MVD） in oral squamous cell carcinoma （OSCC）. Methods： Expressions of Angiopoietin-1 and CD34 in 41 human OSCC tissues, 30 adjacent noncancerous oral tissues and 10 normal oral mucosas were detected by immunohistochemical SABC method. MCD was also assessed. Results： Of the 41 OSCC tissues, 41.46% （17/41） was Ang-1 positive. The expression of Ang-1 was significantly lower in OSCC than that in adjacent noncancerous oral tissues （P〈0.05） and normal oral mucosa （P〈0.05）. The Ang-1 expression was significantly higher in high differentiated tumor than that in moderately differentiated tumor （P〈0.05）. The MVD was significantly higher in Ang-1-negative OSCC than in Ang-1-positive OSCC （P〈0.01）, and negatively correlated with the expression of Ang-1 （r=-0.32, P〈0.05）. Conclusion： Down-regulated expression of Ang-1 may play a crucial role in the development of OSCC. It negatively regulated the angiogenesis of tumor.

Salvianolate Reduces Murine Myocardial Ischemia and Reperfusion Injury via ERK1/2 Signaling Pathways in vivo

Objective： To analyze the effects of salvianolate on myocardial infarction in a murine in vivo model of ischemia and reperfusion （I/R） injury. Metheds： Myocardial I/R injury model was constructed in mice by 30 min of coronary occlusion followed by 24 h of reperfusion and pretreated with salvianolate 30 min before I/R （SAL group）. The SAL group was compared with SHAM （no I/R and no salvianolate）, I/R （no salvianolate）, and ischemia preconditioning （IPC） groups. Furthermore, an ERK1/2 inhibitor PD98059 （1 mg/kg）, and a phosphatidylinositol-3-kinase （PI3-K） inhibitor, LY294002 （7.5 mg/kg）, were administered intraperitoneal injection （i.p） for 30 min prior to salvianolate, followed by I/R surgery in LY and PD groups. By using a double staining method, the ratio of the infarct size （IS） to left ventricle （LV） and of risk region （RR） to LV were compared among the groups. Correlations between IS and RR were analyzed. Western-blot was used to detect the extracellular signal-regulated kinase 1/2 （ERK1/2） and protein kinase B （AKT） phosphorylation changes. Results： There were no significant differences between RR to LV ratio among the SHAM, I/R, IPC and SAL groups （P〉0.05）. The SAL and IPC groups had IS of 26.1% ± 1.4% and 22.3% ±2.9% of RR, respectively, both of which were significantly smaller than the I/R group （38.5% ± 2.9% of RR, P〈0.05, P〈0.01, respectively）. Moreover, the phosphorylation of ERK1/2 was increased in SAL group （P〈0.05）, while AKT had no significant change. LY294002 further reduced IS, whereas the protective role of salvianolate could be attenuated by PD98059, which increased the IS. Additionally, the IS was not linearly related to the RR （r=0.23, 0.45, 0.62, 0.17, and 0.52 in the SHAM, I/R, SAL, LY and PD groups, respectively）. Conclusion： Salvianolate could reduce myocardial I/R injury in mice in vivo, which involves an ERK1/2 pathway, but not a PI3-K signaling pathway.