丁酸钠对人胰腺癌细胞ASPC-1生长的影响及其机制的研究

目的 探讨丁酸钠对人胰腺癌ASPC-1细胞生长的影响并探讨其作用机制.方法 使用不同浓度丁酸钠处理ASPC-1细胞.MTT法观察肿瘤细胞的增殖;流式细胞仪检测细胞凋亡和细胞周期的变化;Western印迹法检测细胞内p21、p53、bcl-2、bax蛋白表达的变化,实时定量PCR检测p21和bcl-2的表达.结果 丁酸钠能明显抑制ASPC-1细胞的增殖,其作用具有明显的时间和剂量依赖性.丁酸钠处理24 h后ASPC-1细胞凋亡率明显提高(P＜0.05),S期细胞比例显著降低(P＜0.05),G0/G1期细胞比例显著升高(P＜0.05).p21、bax蛋白表达明显上调(P＜0.05);bcl-2蛋白的表达显著降低(P＜0.05);p53蛋白表达无明显变化(P＞0.05).结论 丁酸钠可以通过诱导胰腺癌细胞的凋亡和周期阻滞而抑制癌细胞生长;其发生机制可能与下调抗凋亡基因bcl-2、上调促凋亡基因bax和肿瘤抑制基因p21的表达有关.

Abstract：

Objective To investigate the effects of sodium butyrate(NaBT) on proliferation of human pancreatic cancer cell line ASPC-1 and explore the possible mechanism. Methods The methylthiazolyl tetrazolium assay (MTT) method was used to detect cell proliferation and draw a curve. The cell apoptosis and cell cycle were determined with flow cytometry. Western blot was used to study the effect NaBT on the pancreatic cancer cells and explore its mechansim. Real-time PCR was employed to assess the expression levels of p53, p21, bcl-2 and cell cycle regulation gene p21. Results After incubation with different concentrations of NaBT for 24 to 72 h, ASPC-1 cell proliferation was inhibited dramatically. NaBT induced an increase of G0/G1 phase cells and a significant decrease in the ratio of S phase cells. The expression of p21 and bax was up-regulated at protein and mRNA level. The expression of bcl-2 was down-regulated at protein and mRNA level. There was no significant difference in the expression of p53 at protein and mRNA level. Conclusion TSA-induced growth inhibition is associated with a block in the G0/G1 phase and apoptosis, which may occur through down-regulating the expression of apoptosis gene bcl-2 and up-regulating the expression of cell cycle regulation gene p21and pro-apoptotic gene bax.     

带蒂大网膜修补肺结核术后主支气管胸膜瘘

1985年11月～1996年6月,我院采用带蒂大网膜胸腔移植修补肺结核全肺切除术后主支气管胸膜瘘5例,效果满意,报告如下.     

开胸术后不同镇痛方法效果比较

目的比较开胸术后不同镇痛方法的镇痛效果。方法90例开胸术后患者，随机分戍术后应用镇痛药组（A组）、硬膜外置管给药组（13组）及肋间神经冷冻止痛组（C组），比较3组术后镇痛效果，术后并发症及需要辅助应用镇痛方法。结果C组的术后镇痛效果明显优于A组和B组，差异有统计学意义（P〈0．05），并发症较A组和13组明显减少，差异有统计学意义（P〈0．05）。结论肋间神经冷冻止痛是一种可靠的预防开胸术后剧烈疼痛的方法。     

胰岛素对人胰腺癌PANC1细胞增殖与侵袭能力的影响

目的 研究胰岛素对人胰腺癌PANC1细胞增殖、侵袭能力及细胞低氧诱导因子(HIF-1α)、血管内皮生长因子( VEGF)表达的影响.方法 采用0.1、1、10、100 nmol/L胰岛素处理PANC1.噻唑蓝法和Transwell小室侵袭实验检测细胞增殖和侵袭能力;蛋白质印迹法和实时PCR法检测增殖性细胞核抗原(PCNA)及HIF-1α、VEGF蛋白和mRNA的表达.结果 胰岛素呈剂量依赖性诱导PANC1细胞的增殖,上调HIF-1α、VEGF蛋白表达.100 nmol/L胰岛素干预4d,PANC1细胞的PCNA蛋白表达显著上调(1.196±0.014比1.157±0.013,P＜0.05);Transwell小室穿膜细胞数量显著增加[(141.0±2.1)个比(89.0±1.4)个,P＜0.05];HIF-1α蛋白表达显著上调(1.139±0.020比0.598 ±0.013,P＜0.05),但HIF-1α mRNA表达无明显变化;VEGF蛋白表达显著上调(1.011±0.023比0.627±0.013,P ＞0.05),VEGF mRNA表达亦显著上调(0.970±0.016比0.350±0.013,P＜0.05).结论 高胰岛素微环境可诱导PANC1细胞增殖,并通过上调HIF-1α及VEGF的表达增强细胞的侵袭能力.     

Insulin promotes proliferative vitality and invasive capability of pancreatic cancer cells via hypoxia-inducible factor 1α pathway

This study examined whether insulin-stimulated hypoxia-inducible factor 1α(HIF-1α) expression plays a crucial role in promoting the proliferative vitality and invasive capability in human pancreatic cancer cells.PANC-1 cells were divided into three groups:Control group,insulin group and insulin+YC-1(a pharmacological inhibitor of HIF-1α) group in terms of different treatments.Cells in the insulin group or insulin+YC-1 group were treated with insulin(0.1,1,10 and 100 nmol/L) alone or combined with 3-(5'-hydr...