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Objective To establish a cell line of human ovarian cancer, and study its characterization. Methods The cell line was established by the cultivation of subsides walls, and kept by freezing. The morphology was observed by microscope and electromicroscope. The authors studied its growth and propagation, the agglutination test of phytohemagglutinin (PHA), the chromosome analysis, heterotransplanting, immuno histochemistry staining, the analysis of hormone, the pollution examination and the test of sensitivity to virus etc. Results A new human ovarian carcinoma cell line, designated ovarian mucinous cystadenocarcinoma 685 (OMC685), was established from mucinous cystadenocarcinoma. This cell line had subcultured to 91 generations, and some had been frozen for 8 years and revived, still grew well. This cell line possessed the feature of glandular epithelium cancer cell. The cells grew exuberantly, and the agglutinating test of PHA was positive. Karyotype was subtriploid with distortion. Heterotransplantations,alcian blue periobic acid schiff (AbPAS),mucicarmine,alcian blue stainings, estradiol (E 2) and progesterone were all positive. Without being polluted, it was sensitive to poliovirus Ⅰ, adenovirus 7 and measles virus. Conclusions OMC685 is a distinct human ovarian tumous cell line.
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Objective To investigate the role of mitochondrial KATP channel in the mechanism of the protective effect of ischemic preconditioning (IP) against ischemia-reperfusion (I/R) injury.Methods Forty-eight Wistar rats of both sexs weighing 250-350 g were used in this study. Forty rats were randomly divided into 5 groups ( n = 8 each): group A I/R; group B IP+ I/R; group C diazoxide (DZ mito-KATP channel activator) + I/R; group D 5-HD (mito-KATP channel blocker) + IP + I/R and group E 5-HD + DZ + I/R. Another 8 animals were used for electron microscopic examination of normal mitochondria as control. The animals were anesthetized with intraperitoneal pentobarbital 30 mg?kg-1. The hearts were immediately excised and passively perfused in a Langendorff apparatus with K-H solution at 5.8 kPa perfusion pressure and 36.5-37.5℃ via aortic cannulation. A fluid-filled latex balloon was via left atrium in left ventricle for the measurement of left ventricular function. I/R was induced after 30 min stabilization by clamping aortic cannula for 40 min followed by 30 min reperfusion. In group B and D the isolated hearts underwent 2 episodes of 5 min ischemia followed by 5 min reperfusion before I/R. In group C and E DZ 50 ?mol?L-1 was infused for 10 min and in group D and E 5-HD 100 ?mol?L-1 was infused for 10 min before I/R. HR, LVSP, LVEDP and coronary flow (CF) were measured at the end of stabilization (T0 , baseline), immediately before I/R (T1 ) and at 10, 20 and 30 min of reperfusion (T2.3.4.), and left ventricular developed pressure (LVDP= LVSP- LVEDP) was calculated. Myocardial tissue was obtained at the end of 30 min reperfusion for electron microscopic examination of mitochondria. Mitochondrial ultrastructure was assessed by Flameng scoring system (0 = normal, 4 = severely damaged) .Results Ischemic and DZ preconditioning significantly increased LVDP and decreased LVEDP and Flameng score. 5-HD pretreatment partly antagonized the protective effect of IP and completely antagonized that of DZ against I/R injury. Conclusion Ischemic preconditioning protects the heart against I/R injury mainly by activating mitochondrial KATP channel.