高表达P73基因抑制肺腺癌细胞VEGF、bFGF mRNA表达

目的　观察高表达的p73基因对肺腺癌细胞生长曲线以及血管内皮生长因子 (VEGF)、碱性成纤维细胞生长因子 (bFGF)mRNA表达水平的影响 ,探讨高表达 p73基因在肺腺癌血管生成中的作用。 方法　将 p73α、p73 β以脂质体法转染A5 49细胞、H12 99细胞 ,采用细胞计数法绘制转染前后两种细胞生长曲线 ,RT PCR法半定量分析转染前后两种细胞中VEGF、bFGFmRNA的表达水平的变化。结果　转染p73基因后 ,A5 49细胞、H12 99细胞生长受到抑制 ,VEGF、bFGFmRNA表达水平下降 ,较未转染 p73基因的细胞有显著性差异 (P <0 .0 5 ) ,其中 p73 β对VEGFmRNA表达的抑制作用更为显著 (P <0 .0 1)。 结论　高表达的 p73基因能够抑制肺腺癌细胞生长 ,降低肺腺癌细胞中VEGF、bFGFmRNA表达水平 ,提示高表达的 p73基因可能参与调控人肺腺癌VEGF和bFGF基因表达 ,从而起到一个抑癌基因的作用     

Study on the Difference in Expression of VEGF and bFGF and their Receptors in Young and Postmenopausal Women with Breast Cancer

Objective To study the difference in expression of VEGF and bFGF and their receptors in young and postmenopausal women with breast cancer. Methods Immunohistochemical methods (SABC) were used to study the expression of VEGF, FLK-1, bFGF and FLG on paraffin-embedded sections from 40 cases of young and 30 cases of postmenopausal women with breast cancer, The relationship between axillary lymph node metastasis and the expression of the growth factors and their receptors was studied. Results The mean expression of VEGF and bFGF and the positive rate of axillary lymph nodes in the young group were higher than that in the postmenopausal group (P< 0.01 or P< 0.05 ); the mean values of VEGF, bFGF, FLK-1 and FLG in cases of axillary lymph node metastasis were higher in patients without axillary lymph node metastasis in each group (P< 0.05 orP< 0.01); there was a significant difference between the mean expression of VEGF, bFGF, FLK-1 and FLG in cases of stage 0 ∼II comparaed to cases of stage III∼IV (P< 0.05 or P< 0.01). Conclusion The tumor vasculature is directly related to the high breast cancer aggressiveness in young women, a characteristic that might be due to the high expression of VEGF and bFGF.     

Elevated ocular levels of vascular endothelial growth factor in patients with von Hippel-Lindau disease

Background: Von Hippel–Lindau disease (VHL) is a rare autosomal dominant inherited disorder characterized by highly vascularized tumors in various organs. The abundant presence of endothelial cells in VHL tumors strongly suggest a role of the VHL tumor suppressor gene in the regulation of angiogenesis. Recently, in vitro studies have shown that the VHL tumor suppressor gene regulates the expression of vascular endothelial growth factor (VEGF). We investigated whether VHL patiens have increased levels of VEGF in their body fluids.Patients and methods: The concentration of VEGF was measured in fluid of the anterior chamber of the eye, serum, urine, and fluid from renal cysts of VHL patients and unaffected individuals by ELISA. In addition, levels of basic fibroblast growth factor (bFGF), interleukin-8 (IL-8) and endothelin-1 (ET-1) were measured in urine and serum of VHL patients and control subjects.Results: In 80% of the VHL patients VEGF was detectable in aqueous fluid of the anterior chamber of their eyes. A strong positive correlation (r = 0.90) was found between the age of VHL patients and ocular VEGF concentrations. At comparable age, VEGF levels in ocular fluid of VHL patients were significantly higher (P < 0.001) than in unaffected subjects. No correlation was found between VEGF concentration and the presence of retinal angiomas. A 10 and 16 fold increase of VEGF concentration was seen in fluid from two independent VHL-related cysts as compared with VEGF serum levels of the same patient. The mean concentration of VEGF in serum of VHL patients (n = 15) (319 ± 84 pg/ml) was higher than in matched controls (238 ± 68 pg/ml; P = NS). The mean concentration of VEGF in urine of VHL patients (128 ± 36 pg/ml) was lower than in matched controls (183 ± 25 pg/ml; P = NS). Concentrations of VEGF did not correlate with the presence of VHL-related tumors. No differences were observed between concentrations of bFGF, IL-8 and ET-1 in serum and urine of VHL patients and matched controls.Conclusions: These findings support a role for the VHL tumor suppressor gene in the in vivo regulation of VEGF.     

急性白血病患者血清bFGF与TSGF水平的研究

目的探讨急性白血病(AL)患者血清碱性成纤维细胞生长因子(bFGF)及恶性肿瘤相关物质群(TSGF)的水平及其临床意义。方法应用酶联免疫法(ELISA)及化学显色法分别对47例AL初治(AL初治组)、8例AL复发(AL复发组)患者化疗前后血清bFGF及TSGF的水平进行检测,并与正常人对照组比较;47例AL初治患者化疗后,根据疗效观察,其中11例CR(完全缓解组,CR组)、13例NR(未缓解组,NR组),对CR组与NR组患者血清bFGF及TSGF的水平进行对比分析。结果AL初治组及AL复发组血清bFGF水平均明显高于正常人对照组水平,有非常显著性差异(t=6.71、6.18,P均<0.001);AL初治组及AL复发组血清TSGF水平均明显高于正常人对照组水平,差异非常显著(t=6.847、5.009,P均<0.001);CR组血清bFGF水平及TSGF水平均明显下降,与正常人对照组相比较,均无显著性差异(t=1.11、1.482,P均>0.05);ALLNR组化疗前血清bFGF水平明显高于ALLCR组化疗前的水平,具有显著性差异(t=2.43,P<0.05),AMLNR组与AMLCR组化疗前血清bFGF水平无显著性差异(t=0.76,P>0.05);ALL与AMLNR组化疗前血清TSGF水平均高于CR组化疗前的水平,且均具有显著性差异(t=3.29,2.13;P<0.01,0.05);血清bFGF水平与TSGF水平呈正相关(γ=0.5263,P<0.01)。结论联合检测血清bFGF及TSGF水平对了解AL的发生、发展     

中华眼镜蛇毒组分抑制肺癌细胞H1299的血管生长因子VEGF和Bfgf

目的:了解中华眼镜蛇毒活性组分(CCVAF)对人非小细胞肺癌细胞株H1299VEGF、bFGF表达的抑制作用。方法:采用RTPCR方法检测H1299细胞中VEGF、bFGFmRNA表达的变化;利用ELISA检测培养上清中VEGF、bFGF蛋白的含量。结果:不同浓度的(2.0、4.0μg·ml-1)CCVAF对H1299bFGFmRNA水平有降低作用,其中4.0μg·ml-1CCVAF作用7h后bFGFmRNA的表达明显降低,但对VEGFmRNA的表达无明显影响。CCVAF作用H1299细胞24h后,其细胞上清中VEGF、bFGF的含量较对照组明显减少(P<0.05),且呈剂量依赖性。结论:CCVAF可抑制H1299细胞bFGFmRNA和蛋白的表达及VEGF蛋白的表达。     

兔牙周组织在正畸力下bFGF变化的研究

目的 通过检测受正畸力后兔牙周组织压力侧bFGF的表达,了解兔牙受力过程中bFGF在牙周组织的变化情况.方法 将动物分为等量4组,其中一组作为对照,实验组以左、右侧上颌第一磨牙为研究对象,两牙之间施加50克左右的力,3个实验组分3次在受力24小时、1周、2周将动物处死,制备牙体-牙周组织标本,进行免疫组化染色(HI-SABC法)后检测、分析.结果 对照组bFGF染色呈弱阳性,受力24小时组与对照组无显著性差异,受力1周、2周组bFGF染色情况与对照组有显著性差异,3个实验组两两比较差异无显著性.结论 bFGF在正畸牙周组织改建中有一定作用.     

bFGF-PLA缓释纳米微球的制备及体外释药的研究

目的制备bFGF-PLA纳米微球,观察其一般特性、载药量和包封率和缓释特性。方法应用超声乳化法制备缓释bFGF-PLA纳米微球,观察其一般特性,采用ELISA方法测定bFGF含量,并模拟体内条件研究bFGF-PLA纳米微球的体外缓释特性。结果纳米微球表面光滑圆整,球体大小均匀,平均粒径为(0.045±0.013)μm,微球包封率和载药量分别为(91.72±1.31)%和〔(27.65±0.44)×10-3〕%。微球体外释药符合Higuichi方程:突释期仅为18.37%,14d后释放度达75.72%。结论bFGF-PLA纳米微球制备工艺效果满意,具有明显的缓释作用。     

莪术油注射液对小鼠移植性S180肉瘤血管形成的抑制作用

目的 探讨莪术油对肿瘤血管形成抑制作用。方法 通过建立动物肿瘤模型，运用莪术油予以实验治疗，结合免疫组化，检测其抑瘤率和肿瘤内血管密度，以及瘤体VEGF和bFGF表达的改变：结果 莪术油具有明显的抑制S180肉瘤作用，其大剂量组抑瘤率达46．68％。小、中、大剂量实验组的S180瘤体内微血管密度均明显低于对照组；免疫组化显示莪术油大剂量组均可抑制S180瘤体内VEGF，bFGF的表达：结论 莪术油对小鼠S180肉瘤有一定的抑制作用，对肿瘤血管形成均有明显抑制作用，降低VEGF、bFGF的表达可能是其抑制肿瘤血管形成的主要机制之一。     

碱性成纤维细胞生长因子对庆大霉素肾损害保护作用的体外实验研究

目的　研究碱性成纤维细胞生长因子 (bFGF)对庆大霉素引起的体外培养的大鼠肾小管上皮细胞损害的保护作用。方法　大鼠肾皮质经研磨、过网、胰蛋白酶消化,进行肾小管上皮细胞的体外培养。经Cytokeratin18抗体进行鉴定后,用庆大霉素建立损伤模型,观察bFGF对损伤的肾小管上皮细胞的保护作用。结果　①经形态学观察、Cytokeratin18免疫细胞化学方法鉴定;GM组与对照组比较,CAT、Na+,K+ ATP酶活性下降,而NAG活性和MDA升高 (P<0 01),提示肾小管上皮细胞的培养和庆大霉素损伤的建模成功。②bFGF+GM组与GM组比较,各生化和酶学指标差异均有显著性(P<0 01 );而bFGF+GM组与对照组比较,CAT、Na+,K+ ATP酶、NAG酶活性差异无显著性 (P>0. 05 ),但MDA增高差异仍有显著性(P<0 05)。结论　bFGF能保护损伤的肾小管上皮细胞。     

脑脉康对脑缺血再灌注损伤后BDNF、bFGF蛋白表达的影响

新近脑内神经营养因子对脑缺血损伤后神经修复与再生的作用与机制研究成为研究的热点.其中脑源性神经营养因子(BDNF)系脑内分布最为广泛的神经营养因子家族成员之一[1、4],与碱性成纤维细胞生长因子(bFGF)一样在中枢神经系统的发育和成熟,以及新生血管形成方面发挥着重要作用.脑缺血后脑内多种神经营养因子均呈现高表达,与缺血后脑组织蛋白表达的变化及分布规律,探讨中药复方脑脉康的脑保护作用及机制.