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 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.
【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。
Objective To study the relationships between expressions of somatostatin receptor subtypes（SSTR1-SSTR5） and angiogenesis in colorectal cancer. Methods The expressions of SSTR1-SSTR5, VEGF, and CD34 in the paraffin sections of colorectal cancer tissues from 127 cases were detected by the standard streptavidin-peroxidase (SP) technique. CD34 was used as a marker to account microvessel density (MVD) in colorectal cancer tissues. The relationships between the expressions of SSTR1-SSTR5 and VEGF expression, or MVD were analyzed. Results The positive expression rate of SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5 was 64.6% （82/127）, 36.2% （46/127）, 18.9% （24/127）, 18.9% （24/127）, and 38.6% （49/127） in colorectal cancer tissues, meanwhile, the positive expression rate of VEGF was 63.8% （81/127） and MVD was (34.67±16.62)/HP in colorectal cancer tissues. The positive expression rate of VEGF (47.8%， 22/46) and MVD 〔(29.00±15.32)/HP〕 in colorectal cancer tissues with SSTR2 positive expression were significantly lower than those in colorectal cancer tissues with SSTR2 negative expression 〔72.8%， 59/81； (37.90±16.56)/HP〕, Plt;0.05. There were no relationships between SSTR1, SSTR3, SSTR4, and SSTR5 expression and VEGF expression or MVD （Pgt;0.05）. Conclusion The positive expression of SSTR2 is related with angiogenesis in colorectal cancer tissues.
Objective To investigate the effect of angiostatin gene combined with somastatin on inhibiting proliferation of human pancreatic cancer cell BXPC-3 and endothelial cell of vascular ECV-304 and on inducing their apoptosis in vitro. Methods The pcDNA3/angio was transfected BXPC-3 by liposome-mediated gene transfer method. RT-PCR and Western blot were used to detect the expression of angiostatin gene. In vitro, MTT and flow cytometry (FCM) were used to detect whether angiostatin gene combined with somastatin could effect the growth inhibition of BXPC-3 and ECV-304 cells. Results Angiostatin was expressed and secreted by transfected BXPC-3. The growth of BXPC-3 was inhibited by certain concentration of somatostatin (≥10 μg/ml, P＜0.01）, which was dependent on the dose of somatostatin in a concentration extent; Simultaneity apoptosis was induced （P＜0.01）. But the growth of ECV-304 was not inhibited with somatostation （Pgt;0.05）. Angiostatin could inhibit the growth of ECV-304 and induced apoptosis （P＜0.01）, but it had no effect on the growth of BXPC-3 （Pgt;0.05）. Angiostation gene combined with somatostation could inhibit the growth both of BXPC-3 and ECV-304 （P＜0.01）, and induce apoptosis of them （P＜0.01）; but the effect couldn’t be additived. Conclusions ①Somatostatin directly inhibits the proliferation of human pancreatic cancer cells and induces apoptosis, but it doesn’t directly inhibit angiogenesiso of human pancreatic cancer. ②Angiostatin specially inhibits the proliferation of endothelial cell of vascular and induces apoptosis. Angiostatin could inhibit angiogenesis of human pancreatic cancer to induce necrosis of cancer cell.
Objective To systematically evaluate the effectiveness of somatostatin analogs versus placebo for Graves’ ophthalmopathy (GO). Methods Such databases as PubMed, EMbase, The Cochrane Library, WanFang Data, CNKI, VIP and CBM were searched to collect the randomized controlled trails (RCTs) about somatostatin analogs for Graves’ Ophthalmopathy (GO) pulished by March 2012, while the bibliographies of the included literatue were also retrieved. According to the inclusion criteria, two reviewers screened literature, extracted data and assessed the quality of the included studies. Then meta-analysis was conducted using RevMan 5.0 software. Results A total of 5 RCTs involving 210 patients were included. The results of meta-analysis showed that somatostatin analogs could reduce the clinical activity score (CAS) of GO patients (MD=0.58, 95%CI 0.02 to1.13, P=0.04), but the effects in reducing the degree of proptosis (mm) was still unverifiable (MD=0.21, 95%CI –0.14 to 0.56, P=0.24). It did not show obvious effects for diplopia, orbital volume, intraocular pressure, visual acuity or the restriction of eye movements. The existing evidence could not confirm that somatostatin analogs were effective for GO (OR=1.32, 95%CI 0.45 to 3.9, P=0.61). Conclusion Somatostatin analogs can reduce the CAS of GO patients, but without significantly clinical significance. Moreover, the effect of reducing proptosis is sitll unverifiable. So the existing evidence cannot confirm that somatostatin analogs are effective for GO. For the quality and quantity limitation of the included studies, this conclusion needs to be proved by performing more high quality RCTs.
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.
ObjectiveTo detect the effect of adeno-associated-virus induced Kringles5 gene on retinal neovascularization in rats with retinopathy of prematurity (ROP), and to explore the new ways of treatment for ROP.MethodspSNAV-Kringle5-gfp carrier was constructed by subclone and adeno-associated-virus was packed to form rAAV-Kringle5-gfp. ROP model was set up under circumstances of high oxygen in 21 SD rats which were divided into experimental (21 eyes) and control group (21 eyes). Eighteen eyes from each group was used to making the histologic section of retina, and the other 3 eyes in each group was detected by polymerase chain reaction (PCR) and Western blotting. There were 5 rats in the normal control group. AAV-Kringle5-gfp with the dosage of 10 μl and titer of 2.5×1012vg/ml was injected into the eyes in experimental group, while rAAVlacZ with the same dosage and titer of 2.5×1011vg/ml was injected in to the eyes in control group. The expression of target gene in ocular tissues was observed under the fluoroscope. Twelve weeks later, the rats were executed, and the staining of Ⅷ factor related antigens in retinal vascular endothelial cells was performed and number of nucleolus of vascular endothelial cells were counted. ResultsThe plasmid of pSNAV-Kringle5-gfp was correct according to the sequence measurement; the expression of rAAV-Kringle5-gfp was found in vitreous cavity and on retina; the expression of target gene was found on the level of mRNA and protein; the number of nucleolus of vascular endothelial cells on the surface of retina was (19.954 2±3.825 7) in experimental group and (7.335 2±2.731 3) in the control group, which had significant difference between the two groups (P＜0.01）.ConclusionsAdeno-associated-virus induced Kringles5 gene can inhibit the occurrence of retinal neovascularization in patients with ROP.(Chin J Ocul Fundus Dis, 2005,21:288-291)
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.