Objective To study the effects of pcDNA3/AFP/TK/Angio fusion gene targeting therapy for human primary liver cancer in nude mice implanted with SMMC-7721. Methods Human liver cancer cell line SMMC-7721 was implanted subcutaneously in nude mice to establish experiment model. Animals bearing liver cancer were randomly divided into five groups: control group， vector group， GCV (ganciclovir) group， pcDNA3/TK/Angio group; pcDNA3/AFP/TK/Angio group. Different plasmids were directly injected into tumors and GCV was intraperitoneally administrated simultaneously according to different groups. The growth of tumors was observed and the pathology was examined as well. Serum AFP level was measured by radioimmunology, the ultrastructural change of tumor cells was studied by using electron microscopy, the expressions of MVD and VEGF were respectively detected with immunohistochemistry and the cell apoptosis in situ was detected by TUNEL. Results The success rate to establish subcutaneous implanted liver cancer model in nude mice was 100%. The tumor volume, serum AFP level, VEGF and MVD expressions of pcDNA3/TK/Angio group and pcDNA3/AFP/TK/Angio group were lower than those in control group, vector group and GCV group (P＜0.05) and more apoptosis cells could be observed. While the tumor volume, serum AFP level, VEGF and MVD expressions of pcDNA3/AFP/TK/Angio group was lower than those in pcDNA3/TK/Angio group (P＜0.05); and apoptosis index was higher than that of the latter (P＜0.05).Conclusion pcDNA3/AFP/TK/Angio fusion gene inhibits the growth of tumor remarkably and becomes a promising new biological agent to treat human primary liver cancer.
The model of transplanted colonic SW480 cell line carcinoma in gymnomouse body was set up to observe the effect of octapeptide somatostatin (SMS 201-995,SMS) on the transplanted carcinoma and elucidate its mechanism. Results: the volume, weight, DNA and protein content in carcinoma cell, cell amount and proliferation index of S and G2M phase in SMS group and SMS+PG (pentagastrin) group were markedly lower than those in PG group and control group, those of PG group were markedly higher than those in control group.The cell amount of G0/G1 phase in SMS group and SMS+PG group was markedly higher than that in PG group and control group, and that of PG group was markedly lower than that in control group.All these suggested that somatostatin could not only inhibit the growth of transplanted human colonic SW480 cell line carcinoma directly but also inhibit the growthpromoting effect of gastrin on the transplanted carcinoma.The mechanism might be that somatostatin inhibit the synthesis of cAMP, DNA and protein in carcinoma cells, then inhibit the cell growing from G0/G1 phase to S and G2M phases.Our study might provide experimental basis for the homonotherapy with analogue of somatostatin in patients with large intestine carcinoma.
目的 探讨生长抑素-14肽与生长激素联合应用在预防胰十二指肠切除术后并发症发生中的作用。方法 我院1995年3月至2003年3月共收治因胆总管下段癌、十二指肠乳头癌及胰头癌行胰十二指肠切除术患者48例，对其中26例（治疗组）应用生长抑素-14肽6 mg/d（持续微量泵泵入）及生长激素8 U/d（分两次肌注）治疗，余22例为对照组，术后常规应用全肠外营养及抗生素治疗，比较两组的治疗结果。结果 术后发生并发症对照组17例（77.3%），治疗组5例（19.2%），两组比较差异有显著性意义（P＜0.05）。治疗组胰液量及胰周引流液中淀粉酶的含量明显低于对照组（P＜0.05），两组术前、术后蛋白质指标，治疗组于术后第7天基本恢复到术前水平，而对照组第10天才达到术前水平。结论 联合应用生长抑素及生长激素能有效降低胰十二指肠切除术后并发症的发生率。
【Abstract】ObjectiveTo investigate the inhibitory effects of somatostatin analogue (SSTA) on the colonic carcinoma cell growth in vitro and in vivo and its possible mechanism. MethodsThe somatostatin receptor type Ⅱ (SSTR2) mRNA of colonic carcinoma cell line HCT116 was detected by using RTPCR and hybridization in situ. The effects of octreotide (Oct) or NC-8-12 (specific agonist of SSTR2 ) on the proliferation of HCT116 was measured with MTT after HCT116 stimulated by insulin or epidermal growth factor (EGF) and incubated with Oct or NC-8-12 simultaneously for 24 hours. The expression of cyclin D1 was detected with flow cytometry. The HCT116 were implanted in nude mice subcutaneously and treated with Oct or NC-8-12. The tumor volume and tumor weight were measured according to schedule. Results①SSTR2 mRNA was detected in HCT116 and the tumor implanted in nude mice; ②Insulin and EGF increased the proliferation of HCT116 significantly, and this proliferation could be inhibited by Oct and NC-8-12 partially; ③Insulin increased the Cyclin D1 expression of HCT116, its level decreased slightly when treated with Oct or NC-8-12 but not significantly (Pgt;0.05); ④The weight and volume of implanted tumor in nude mice treated with Oct or NC-8-12 showed no significant difference compared with the control group (Pgt;0.05). ConclusionBoth Oct and NC-8-12 could inhibit the proliferation of colonic carcinoma cell line HCT116 in vitro, which indicated that SSTR2 may mediated the inhibition. Oct and NC-8-12 have no effect on the growth of implanted HCT116 in nude mice in this experiment.
Objective To investigate the regulatory effect of somatostatin analogue (SMS201995,SMS) on proliferation and apoptosis in human cholangiocarcinoma cell line in vitro. MethodsProliferation curve, flow cytometry, agarose gel electrophoresis, Annexin VFITC and flow cytometric immunofluorescent technique were performed to identify the inhibitory effect on cell proliferation and the induction of apoptosis of human cholangiocarcinoma cells (SKChA1). ResultsSMS significantly reduced the SKChA1 cell growth by serum in long experiments and transiently accumulated it in G0/G1 phase. Dotplot analysis of cells duallabeled with Annexin VFITC and PI confirmed the induction of apoptosis by SMS in SKChA1 cells.AnnexinVFITC labeling was markedly enhanced following treatment with SMS for 24 h. DNA of treated SKChA1 cells appeared a ladder pattern characteristic of apoptosis. Besides, timedependent increase in bax and decrease in bcl2 occured during SMS treatment. Conclusion SMS could inhibit the proliferation activity and induce apoptosis of cholangiocarcinoma cell line SKChA1. The mechanisms of apoptosis might be correlated with the expression of apoptosisregulatory gene bax and bcl2.
目的观察特利加压素联合生长抑素治疗肝硬变门静脉高压食管胃底曲张静脉破裂出血的效果。 方法我院2008年3月至2012年8月期间收治的47例肝硬变门静脉高压食管胃底曲张静脉破裂出血患者入院时采用掷硬币法被随机分为特利加压素＋生长抑素组（n=24）和生长抑素组（n=23），分别给予联合用药或单独使用生长抑素，计算24 h止血率、总止血率、1周再出血率、1周死亡率，观察不良反应发生、尿量及腹水量情况。 结果特利加压素＋生长抑素组24 h止血率、总止血率和不良反应发生率明显高于生长抑素组（P＜0.05），1周再出血率明显低于生长抑素组（P＜0.05），2组1周死亡率比较差异无统计学意义（P＞0.05），特利加压素＋生长抑素组尿量明显多于生长抑素组（P＜0.05），盆腔腹水量明显少于生长抑素组（P＜0.05）。 结论特利加压素联合生长抑素用于肝硬变门静脉高压食管胃底曲张静脉破裂出血止血效果确切，可以明显降低死亡率；虽然其不良反应发生率略高，但均可以控制。
【Abstract】ObjectiveTo investigate the inhibitory effects and the mechanisms of octreotide (OCT) on the growth of hepatocellular carcinoma (HCC). MethodsBel7402 HCC cells were studied for proliferative ability by MTT assay, morphology by light microscopy, adhesive and invasive ability by cell adhesion and “wound strack” experiments. Immunofluorescence flow cytometry was used for study of cMet expression and cell cycle as well. Furthermore, the effects of OCT on tumor growth metastasis were investigated in nude mice with implanted HCC. The expression of cMet in implanted tumor cells was studied by immunohistochemistry. ResultsWith OCT treatment, the proliferative ability of Bel7402 cells and cell morphology didn’t change. The adhesive and invasive ability decreased compared with no OCT treatment cells (P＜0.05). The ratio of G0/G1 cells increased markedly (P＜0.05). The proportion of Bel7402 cells expressing cMet was reduced significantly (P＜0.05). The growth of implanted tumor was inhibited with OCT treatment (P＜0.05). The intensity of cMet expression in OCT group was remarkably weaker than that in control group. In addition, no recurrence and metastasis was found in OCT group 7 weeks after curative resection of xenografts, while 3 cases in controd group were observed to have the recurrence and metastasis. The intensity of cMet immunolabeling in the metastatic tumors was higher than that in xenografts of control group, but the difference was not significant. ConclusionOCT inhibits the growth of HCC by downregulation of cMet.
The somatostatin levels in serum, cancer tissue and its adjacent mucosas were measured in 43 patients with large intestine carcinoma(LIC). The results showed that the somatostatin level in serum of patients with LIC before operation was obviously lower than that in the control group (Plt;0.001)and after radical operation, it was markedly higher than the preoperative levels(Plt;0.01), but still lower than the control value(Plt;0.001). The somatostatin level in cancer tissue was evidently lower than that in its adjacent mucosas(Plt;0.001)and in normal mucosa(Plt;0.001). There was no significant correlation between the somatostatin level in serum or carcinoma tissue and Duke’s stage or pathological types of the carcinoma tissue. The results indicate that the somatostatin has a negative modulating effect on the growth of large intestine carcinomas, thus provides an experimental basis for the treatment of large treatment of large intestine carcinomas with drugs such as somatostatin.
【摘要】目的探讨生长抑素(somatostatin,SS)和表皮生长因子(epidermal growth factor,EGF)在银屑病治疗中的相互作用机制。方法选择2008年1月12月门诊和住院的寻常型银屑病患者68例,用放射免疫法检测正常组织和各期银屑病皮损中SS和EGF的表达。结果进行期银屑病皮损中EGF明显高于静止期、恢复期皮损和正常皮肤(P＜001);各期银屑病皮损与正常皮肤中SS差异无统计学意义(P＜005)。结论SS可能是通过抑制EGF而在银屑病的治疗中起关键作用。