AIM: To investigate the protective effect and mechanisms of di-ao-xin-xue-kang (DK) on myocardial ischemia-reperfusion. METHODS: Models of myocardial ischemia-reperfusion were constructed with sixteen mongrel dogs. The left ventricular pressure (LVSP), the marximal/minimum rate of LVSP (?dp/dt max) and the serum aspartate aminotransferase (AST), creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA) were determined before and 90 minutes after occlusion, 120 and 240 minutes after reperfusion, and the MDA content in myocardial cell membrane prepared at 240 minutes after reperfusion was determined. The oxygen free radical was assayed with electron spin resonace spectroscopy (ESR) technique. RESULTS: ① LVSP and ?dp/dt max in the normal saline control (NS) group decreased with the time progress of occlusion-reperfusion, and it was the same in DK group, but the levels were significantly higher than that in NS group (P

Objective:Calcium/calmodulin-dependent kinase kinase (CAMKK2) is activated in prostate cancer (PCa). The aim of our study is to identify the effects of preadipocyte and CAMKK2 on the PCa cell invasion.Methods:The coculture system between PCa cells and preadipocyte cells (3T3L1) was established and then Transwell assay was used to determine the invasive effect after coculture. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to investigate the CAMKK2 expression in the coculture system.Results:The 3T3L1 cells promoted the invasion of PCa cells (DU145 and 22RV1; P<0.01). Meanwhile, the 3T3L1 cells can increased expression of CAMKK2 in PCa cells ( P<0.01). CAMKK2 reversed the invasive effects of preadipocyte cells on the PCa cells. Conclusions:Our study demonstrates that the preadipocyte may promote the PCa cell invasion possibly by mediating the CAMKK2 expression.