Basic Fibroblast Growth Factor and Fibroblast Growth Factor Receptor-1 in Human Meningiomas

The expression of basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor-1 (FGFR-1) in human meningiomas and the relationships between their expression and the tumors' histological features and angiogenesis were investigated by means of immunohistochemical technique. The expression of bFGF and FGFR-1 was detected by antibody of bFGF or FGFR-1. The tumors' angiogenesis was evaluated by microvascular density (MVD) and, which was observed by use of CD34-antibody immunohistochemically. The results showed that there were varied degrees of the expression of bFGF and FGFR-1 proteins in meningiomas. The expression was correlated with the tumors' histological characters and angiogenesis. It was concluded that bFGF and FGFR-1 might play important roles in meningiomas' angiogenesis and proliferation. The expression positive rate of bFGF and FGFR-1 may provide an indication of evaluating the histological and malignant degree of the tumor.

Effect of Ligustrazine on Expressions of Basic Fibroblast Growth Factor and Its Receptor in Bone Marrow of Mice with Acute Radiation Injury

Objective: To study the expressions of basic fibroblast growth factor (bFGF) and its receptor (bFGFR) in bone marrow of mice with acute radiation injury, and to evaluate the effect of Ligustrazine (Lt) on them. Methods: Fifty-six Kunming mice of clean grade were randomly divided into 3 groups, the normal group, the control group and the Lt group. Mice in the latter two groups were once homogeneously systemic irradiated with 6.0 Gy of 60 Co, with the absorption dose rate of 0. 56 Gy/min, then treated with saline (0.2 ml/ mice) or Lt (2 mg/mice) respectively, twice a day through gastrogavage for successive 13 days. Mice were sacrificed in batch on the 3rd, 7th and 14th day by cervical dislocation to collect the bilateral femoral bone marrow for preparing bone marrow mono-nuclear cell (BMMNC) suspension. The bFGFR expression on surface of BMMNC was determined by flow cytometry; and the bFGF expres-sion level in one side of femoral bone marrow tissue was detected by immunohistochemistry with SABC-AP assay. Results: The bFGF expression in bone marrow of mice on the 3rd, 7th and 14th day after acute radiation injury all were significantly lower than that of the normal mice (P<0.05 or P<0.01). The expressions of bFGF and bFGFR in the Lt group detected were significantly higher than that in the control group detected at the corresponding time points (P<0.05 or P < 0.01). Conclusion:By way of enhancing bFGF expression in bone marrow and bFGFR expression on surface of BMMNC to accelerate the repairing of hemopoietic micro-environment in bone marrow might be one of the mechanisms of Lt in promoting hemopoietic function reconstitution after acute radiation injury.Original article on CJITWM (Chin) 2004;24(5):439

EXPRESSION AND SIGNIFICANCE OF BASIC FIBROBLAST GWOWTH FACTOR AND FIBROBLAST GROWTH FACTOR RECEPTOR-1 IN OVARIAN EPITHELIAL NEOPLASM

Objective To study the relevance of expression of basic fibroblast growth factor (bFGF), fibroblast growth factor receptor 1 (FGFR 1) and carcinogenesis and progression of ovarian epithelial neoplasm. Methods Ten cases of normal ovarian tissues and 75 cases of ovarian epithelial neoplasm tissues were detected by immunohistochemical methods: S P for bFGF, FGFR 1,double immunohistochemistry Lab SA for Ki 67 antigen and bFGF. Results The expression level of bFGF, FGFR 1in ovarian epithelium and ovarian epithelial neoplasm showed a step wise increase in the following order:normal <benign <borderline <malignant; The expression level and intensity of bFGF and FGFR 1 were increased with the decrease of differentiation degree and increase of clinical stage in ovarian carcinoma; There was no statistical difference between the expression of bFGF, FGFR 1 in serous cystadenocarcinoma and that of mucinous cystadenocarcinoma; The expression of bFGF was correlated with that of FGFR 1 in neoplastic tissues; There were positive expression rates of bFGF and Ki 67 antigen in ovarian epithelial neoplasm. Conclusion As an important proliferative factor, bFGF plays an important role in carcinogenisis and progression of ovarian epithelial neoplasm.

Basic fibroblast growth factor increases the numbe of endogenous neural stem cells and inhibits the expression of amino methyl isoxazole propionic acid receptors in amyotrophic lateral sclerosis mice

This study aimed to investigate the number of amino methyl isoxazole propionic acid （AMPA） receptors and production of endogenous neural stem cells in the SOD1 G93AG1H transgenic mouse model of amyotrophic lateral sclerosis, at postnatal day 60 following administration of basic fibroblast growth factor （FGF-2）. A radioligand binding assay and immunohistochemistry were used to estimate the number of AMPA receptors and endogenous neural stem cells respectively. Results showed that the number of AMPA receptors and endogenous neural stem cells in the brain stem and sensorimotor cortex were significantly increased, while motor function was significantly decreased at postnatal days 90 and 120. After administration of FGF-2 into mice, numbers of endogenous neural stem cells increased, while expression of AMPA receptors decreased, whilst motor functions were recovered. At postnatal day 120, the number of AMPA receptors was negatively correlated with the number of endogenous neural stem cells in model mice and FGF-2-treated mice. Our experimental findings indicate that FGF-2 can inhibit AMPA receptors and increase the number of endogenous neural stem cells, thus repairing neural injury in amyotrophic lateral sclerosis mice.

^(125)I-labeled anti-b FGF monoclonal antibody inhibits growth of hepatocellular carcinoma

AIM: To investigate the inhibitory efficacy of 125I-labeled anti-basic fibroblast growth factor (bFGF) monoclonal antibody (mAb) in hepatocellular carcinoma (HCC).METHODS: bFGF mAb was prepared by using the 1G9B9 hybridoma cell line with hybridization technology and extracted from ascites fluid through a Protein G Sepharose affinity column. After labeling with 125I through the chloramine-T method, bFGF mAb was further purified by a Sephadex G-25 column. Gamma radiation counter GC-1200 detected radioactivity of 125I-bFGF mAb. The murine H22 HCC xenograft model was established and randomized to interventions with control (phosphate-buffered saline), 125I-bFGF mAb, 125I plus bFGF mAb, bFGF mAb, or 125I. The ratios of tumor inhibition were then calculated. Expression of bFGF, fibroblast growth factor receptor (FGFR), platelet-derived growth factor, and vascular endothelial growth factor (VEGF) mRNA was determined by quantitative reverse transcriptase real-time polymerase chain reaction.RESULTS: The purified bFGF mAb solution was 8.145 mg/mL with a titer of 1:2560000 and was stored at -20 °C. After coupling, 125I-bFGF mAb was used at a 1: 1280000 dilution, stored at 4 °C, and its specific radioactivity was 37 MBq/mg. The corresponding tumor weight in the control, 125I, bFGF mAb, 125I plus bFGF mAb, and 125I-bFGF mAb groups was 1.88 ± 0.25, 1.625 ± 0.21, 1.5 ± 0.18, 1.41 ± 0.16, and 0.98 ± 0.11 g, respectively. The tumor inhibition ratio in the 125I, bFGF mAb, 125I plus bFGF mAb, and 125I-bFGF mAb groups was 13.6%, 20.2%, 25.1%, and 47.9%, respectively. Growth of HCC xenografts was inhibited significantly more in the 125I-bFGF mAb group than in the other groups (P < 0.05). Expression of bFGF and FGFR mRNA in the 125I-bFGF mAb group was significantly decreased in comparison with other groups (P < 0.05). Groups under interventions revealed increased expression of VEGF mRNA (except for 125I group) compared with the control group.CONCLUSION: 125I-bFGF mAb inhibits growth of HCC xenografts. The coupling effect of 125I-bFGF mAb is more effective than the concomitant use of 125I and bFGF mAb.

糖尿病合并慢性难愈合创面患者血清VEGF、bFGF和创面组织EGFR的表达及其临床意义

目的探讨糖尿病合并慢性难愈合创面患者血清血管内皮细胞生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)和创面组织表皮生长因子受体(EGFR)的表达及其临床意义。方法回顾性选取2020年1月至2022年1月联勤保障部队第九〇九医院(厦门大学附属东南医院)收治的糖尿病合并慢性难愈合创面患者76例纳入难愈组,另选取同期接受治疗的糖尿病创面良好愈合的76例患者纳入康复组。对比两组患者治疗前血清VEGF、bFGF及创面组织EGFR的表达水平,分析3项指标表达水平与患者创面难愈的关系;对难愈组患者开展专项治疗,统计临床疗效及创面闭合指数,分析3项指标与难愈组患者临床疗效、闭合指数的相关性。结果治疗前,难愈组患者血清VEGF、bFGF及创面组织EGFR的表达水平分别为(184.69±35.83)pg/mL、(300.24±33.62)pg/mL、(5.67±1.01)分,均低于康复组[(206.01±42.03)pg/mL、(327.91±45.74)pg/mL、(8.20±1.11)分],差异均有统计学意义(P<0.05)。Logistic分析显示,血清VEGF、bFGF及创面组织EGFR均为糖尿病合并慢性难愈合创面的保护因素(P<0.05),且血清VEGF、bFGF及创面组织EGFR联合检测可提高诊断价值(P<0.05)。难愈组治疗1个疗程后临床治愈35.53%,显效40.79%,闭合指数为(81.95±8.48)%;血清VEGF、bFGF及创面组织EGFR与糖尿病合并慢性难愈合创面患者临床疗效间具有高度负相关性(r=-0.938、-0.938、-0.938,P<0.05),与创面闭合指数间均具有高度正相关性(r=0.984、0.983、0.987,P<0.05)。结论血清VEGF、bFGF及创面组织EGFR的表达水平为糖尿病合并慢性难愈合创面的保护因素,较高的血清VEGF、bFGF及创面组织EGFR表达水平有利于降低糖尿病创伤患者并发慢性难愈合创面,且联合检测三项指标对糖尿病合并慢性难愈合创面具有较高的诊断价值。同时糖尿病合并慢性难愈合创面患者3项指标表达水平越高则临床疗效越理想,创面闭合指数亦随着3项指标水平的升高而升高。

乐伐替尼对甲状腺癌SW579细胞放射敏感性及血管内皮生长因子、碱性成纤维细胞生长因子、碱性成纤维细胞生长因子受体表达的影响

目的:探究乐伐替尼对甲状腺癌SW579细胞放射敏感性以及对血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF)及其受体(bFGFR)表达的影响。方法:体外培养甲状腺癌SW579细胞,筛选最佳放射剂量,取培养至对数生长期的SW579细胞分为对照组(常规培养SW579细胞)、放射组(使用4 Gy X射线照射SW579细胞)、乐伐替尼低(在含SW579细胞的培养基中加入5μmol/L的乐伐替尼后,再使用4 Gy X射线照射SW579细胞)、高(在含SW579细胞的培养基中加入10μmol/L的乐伐替尼后,再使用4 Gy X射线照射SW579细胞)浓度组,培养48 h后。检测SW579细胞存活率、细胞凋亡率和细胞中B细胞淋巴瘤-2相关X(Bax)、B细胞淋巴瘤-2(Bcl-2)、活化胱天蛋白酶3(Cleaved caspase-3)、VEGF、bFGF、bFGFR蛋白表达。结果:随着放射剂量的升高,SW579细胞存活率依次降低(均P<0.05),选取4 Gy X射线进行后续实验;与对照组相比,放射组、乐伐替尼低、高浓度组SW579细胞存活率、Bcl-2、VEGF、bFGF、bFGFR蛋白表达依次降低(均P<0.05),细胞凋亡率、Bax、Cleaved caspase-3蛋白表达依次升高(均P<0.05)。结论:乐伐替尼能增强SW579细胞的放射敏感性,其机制可能与抑制VEGF、bFGF、bFGFR蛋白表达有关。

原发性急性闭角型青光眼患者房水中CXCR2和bFGF表达与小梁切除术后预后的关系

目的:探讨原发性急性闭角型青光眼(APACG)患者的房水中趋化因子受体2(CXCR2)、碱性成纤维细胞生长因子(bFGF)水平与小梁切除术后预后的关系。方法:收集2020-06/2022-01期间本院收治的80例80眼行小梁切除术的APACG患者纳入病例组,依据术后疗效分为成功组60例60眼和失败组20例20眼;收集同期本院行白内障超声乳化术且眼压正常的白内障患者86例86眼纳入对照组。采用酶联免疫吸附法检测房水中CXCR2、bFGF水平;采用ROC曲线分析房水中CXCR2、bFGF水平预测APACG患者小梁切除术失败的价值;APACG患者小梁切除术失败的影响因素采用多因素Logistic回归分析。结果:病例组房水中CXCR2、bFGF水平显著高于对照组(P<0.05)。失败组房水中CXCR2、bFGF水平及术后浅前房发生患者比例显著高于成功组(P<0.05)。房水中CXCR2、bFGF水平单独及联合预测APACG患者小梁切除术后失败的AUC分别为0.885、0.883、0.953。CXCR2、bFGF是APACG患者小梁切除术后失败的危险因素(P<0.05)。结论:APACG患者房水中CXCR2、bFGF水平显著升高,且二者均是小梁切除术后失败的危险因素。

艾灸对血管性痴呆大鼠海马内VEGF、flt-1、bFGF及bFGF-r表达的影响

目的观察艾灸对血管性痴呆(vascular dementia,VD)大鼠海马内血管内皮生长因子(vascular endothelial growth factor,VEGF)、fam样酪氨酸激酶-1(fms-like tyrosine kinase-1,flt-1)、碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF),和碱性成纤维细胞生长因子受体(basic fibroblast growth factor receptor,bFGF-r)的表达水平的影响,研究灸法在治疗血管性痴呆中的促血管生成机制。方法选取Wistar雄性老年大鼠,双侧颈总动脉缺血再灌注-硝普钠注射法制备大鼠血管性痴呆模型,电脑随机数字表法随机分为3组:艾灸组、西药组、模型组,并设假手术组对照。艾灸组取百会、大椎、神庭穴艾灸治疗,西药组茴拉西坦灌胃,15天为1个疗程,均为2个疗程。神经行为学评分并结合跳台仪检测治疗前、第2疗程后学习记忆成绩;免疫组化检测各组大鼠海马VEGF、bFGF及其受体flt-1、bFGF-r的表达。结果经2个疗程治疗后,动物跳台实验的潜伏期、错误次数及神经行为学评分,艾灸组及西药组与模型组比较差异有统计学意义(P<0.01,P<0.05),艾灸组与西药组比较潜伏期及神经行为学评分差异也有统计学意义(P<0.05)。表明艾灸、西药在提高VaD大鼠潜伏期,降低VaD大鼠错误次数以及对神经行为学评分影响均有显著疗效,而艾灸组明显优于西药组(P<0.01,P<0.05)。艾灸组及西药组与模型组比,海马内表达VEGF、flt-1、bFGF的灰度值差异均有统计学意义,bFGF-r的表达仅艾灸组与模型组比较差异有统计学意义;VEGF、flt-1艾灸组与西药组比较差异有统计学意义(P<0.05)。结论艾灸在改善VD大鼠行为学评分及提高记忆成绩均有确切疗效,其作用机制可能存在着艾灸调控VD大鼠海马内VEGF、flt-1、bFGF和bFGF-r的表达水平,特别是上调关键因子VEGF、flt-1表达,促进了要害部位的血管生成,并最终激发了脑内神经的损伤修复机制。

川芎嗪对急性放射损伤小鼠骨髓碱性成纤维细胞生长因子及其受体表达水平的影响

目的 探讨急性放射损伤小鼠骨髓碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)及其受体(basic fibroblast growth factor receptor,bFGFR)的表达及川芎嗪对其影响。方法 56只清洁级昆明小鼠,随机分为3组:正常组,急性放射损伤对照组,川芎嗪组。将对照组和川芎嗪组小鼠用6.0Gy60Corγ射线一次性全身均匀照射,吸收剂量率为0.56Gy/min。照射后即分别胃饲生理盐水0.2ml/只及川芎嗪2mg/只,每天2次,连续13天。分别于照射后第3、7、14天颈椎脱臼法处死小鼠,取双侧股骨骨髓细胞制备单个核细胞(bone marrow mono-nuclear cells,BMMNC)悬液,用流式细胞仪检测小鼠BMMNC表面bFGFR的表达水平;取单侧肱骨切片后用免疫组织化学sABC-AP法检测小鼠骨髓组织中bFGF的表达水平。结果 急性放射损伤后第3、7、14天,对照组、川芎嗪组小鼠骨髓组织中bFGF表达显著低于正常组(P<0.05或P<0.01),同一时间点川芎嗪组bFGF、bFGFR的表达均显著高于对照组(P<0.05或P<0.01)。结论 川芎嗪通过促进骨髓组织中bFGF、BMMNC表面bFGFR的表达加速骨髓造血微环境的修复,可能是川芎嗪促进急性放射损伤后骨髓造血重建机制之一。

bFGF,bFGFR及Egr-1基因蛋白在大鼠局灶性脑缺血后的表达

观察持续性局灶性脑缺血 (permanentmiddlecerebralarteryocclusion ,pMCAO)损伤后表达碱性成纤维细胞生长因子 (basicfibroblastgrowthfactor,bFGF)的细胞种类、时相与不同细胞之间的相互影响 ,并探讨Egr 1基因蛋白对bFGF表达的影响。结果表明 :在持续性局灶性脑缺血后 ,缺血梗死灶周边区免疫组化结果显示bFGF表达出现双相增强。缺血 1h缺血边缘区主要在星形胶质细胞 (Astrocyte,As)中bFGF出现一过性增强 ,并见细胞外基质中出现bFGF点状着色。缺血 6h～ 1d时bFGF染色再次增强 ,神经元及各类胶质细胞中的表达均有增强。但是经Western blot定量测定发现脑组织bFGF含量仅在缺血后 6h～ 1d时出现增强。缺血 1h时 ,bFGF可能经缺血细胞受损的细胞膜到达细胞外 ,与细胞外硫酸肝素或相关分子结合 ,内化进入缺血边缘区细胞 ,从而造成bFGF免疫组化染色一过性增强。第二次增强可能是缺血损伤刺激及内化的bFGF诱导的蛋白合成的增加。缺血 2～ 6hbFGFR在神经元及各类胶质细胞中的表达均增强 ,主要位于缺血区的边缘。由于bFGFR表达时程早于bFGF转录合成增加 ,因此限制了内源性bFGF发挥保护缺血损伤神经元的作用 ,这使得外源应用bFGF成为必要。Egr 1基因蛋白的表达在缺血损伤后 1～ 6h增强 ,其表达增高的时相早于bFGF?

壳聚糖对胃溃疡大鼠部分生长因子表达的影响

目的:观察壳聚糖对大鼠消化性溃疡愈合的影响,进而阐明其抗溃疡的可能机制。方法:采用冰乙酸胃窦部浆膜下注射法制备大鼠消化性溃疡模型。70只实验大鼠被随机分成7组,分别为假手术对照组、模型对照组、泮托拉唑治疗组、硫糖铝混悬液治疗组及3个不同剂量(0.25、0.5、1.0g/kg)壳聚糖治疗组。按Guth标准记分判定溃疡指数并计算溃疡抑制率;HE染色观察组织结构。用ELISA法测血清表皮生长因子(EGF);采用免疫组织化学检测鼠胃黏膜表皮生长因子受体(EGFR)及碱性成纤维生长因子(bFGF)的含量。结果:壳聚糖治疗组与模型对照组比较溃疡指数明显降低,溃疡抑制率升高(P<0.01);胃黏膜EGFR及bFGF表达较模型对照组及假手术对照组明显增加(IOD值P<0.05)。0.25g/kg壳聚糖治疗组血清EGF含量最高,与模型对照组、假手术对照组及其他治疗组比较差异均有显著性(P<0.01)。结论:壳聚糖可促进冰乙酸溃疡大鼠的溃疡愈合,并呈一定的量效关系。其促进溃疡愈合作用可能与提高胃溃疡大鼠血清EGF的含量及胃黏膜EGFR及bFGF的表达有关。

乳腺癌VEFG ,bFGF及其受体的表达和与微血管计数的关系(英文)

目的 探讨乳腺癌VEGF ,bFGF及其受体的表达特征和与微血管计数的关系。方法 SABC免疫组化法检测 70例乳腺癌组织中VEGF ,FLK - 1,bFGF ,FLG阳性系数值和MVC值 ,探讨其与腋窝淋巴结转移、临床病理特征之间的关系。结果 腋窝淋巴结转移组VEHF ,bFGF ,FLK - 1,和MVC值明显高于腋窝淋巴结未转移组 ,有非常显著性差异 (P <0 .0 1)。VEGF ,FLK - 1,FLG和MVC值临床分期 0～Ⅱ期和Ⅲ～Ⅳ期组间有显著性或非常显著性差异 (P <0 .0 5或P <0 .0 1)。VEGF ,bFGF表达与MVC的表达呈高度正相关 ,VEGF和bFGF ,VEGF和FLK - 1,bFGF和FLG表达呈相关。结论 乳腺癌VEGF ,bFGF及其受体与肿瘤血管生成、淋巴转移密切相关 ;VEGF ,bFGF可以促进其受体的表达 ;VEGF的表达与bFGF高表达有关。

碱性成纤维细胞生长因子及其受体在人牙髓中的表达

目的 :探讨碱性成纤维细胞生长因子及其受体在人牙髓中表达和意义。方法 :用免疫组化方法检测碱性成纤维细胞生长因子及其受体在人牙髓中的表达。结果 :碱性成纤维细胞生长因子在成牙本质细胞层强阳性表达 ,在牙髓其它细胞和血管内皮细胞阳性表达 ;碱性成纤维细胞生长因子受体在成牙本质细胞层弱阳性表达 ,牙髓其它细胞为阴性。结论

增生性瘢痕形成和成熟过程中c-fos、c-jun和碱性成纤维细胞生长因子基因表达的变化

目的 :探讨c -fos,c -jun和碱性成纤维细胞生长因子 (bFGF)及其受体 (bFGFR2 )在不同形成时期的增生性瘢痕中的基因表达变化规律。方法 :提取 16例不同发生时期的增生性瘢痕和 8例正常皮肤的总RNA后 ,分离mRNA ,用RT -PCR方法检测这 4种基因在不同组织中的表达。结果 :在正常皮肤中 ,c -fos,c -jun ,bFGF和bFGFR基因表达较低 ,而在生长活跃的增殖期的瘢痕中 ,这 4种基因表达水平与正常皮肤相比显著升高 (P <0 .0 5 ) ;在成熟期的瘢痕组织中 ,虽然bFGF基因仍保持高水平表达 ,但c -fos ,c -jun和bFGFR2基因的表达量都明显低于增殖期的瘢痕。结论 :c-fos,c -jun和bFGF及其受体基因表达增强可能是增生性瘢痕形成的机制之一 ,而bFGFR及其下游信使分子基因表达降低 。

碱性成纤维细胞生长因子及其受体在神经管畸形发生中作用的研究

用免疫组织化学方法研究了碱性成纤维细胞生长因子及其受体在正常金黄地鼠和过量维生素Ａ酸致畸金黄地鼠胚胎神经管及其周围间充质的分布状况。结果：碱性成纤维细胞生长因子及其受体广泛分布于正常神经上皮及其内、外界膜和周围间充质中；实验组在服药２２小时后，上述各部位碱性成纤维细胞生长因子及其受体的含量均明显减少。说明碱性成纤维细胞生长因子及其受体与神经管正常发生密切相关；其含量的减少可能是过量维生素Ａ酸致神经管畸形的机制之一。

大鼠液压冲击脑损伤后bFGF及其受体FGFR1的表达

目的观察脑损伤后碱性成纤维细胞生长因子(bFGF)及其受体FGFR1的表达及其时序性变化,探讨脑损伤的分子机制及法医学脑损伤时间推断。方法用免疫组织化学技术观察大鼠侧位中度液压冲击脑损伤后bFGF及FGFR1蛋白在伤后不同时间(30min,1,3,6,12h,1,3,7d)的表达情况,以正常大鼠及手术大鼠作为对照。结果正常对照组和手术对照组大鼠脑组织内有低水平的bFGF和FGFR1表达。脑冲击伤后6h,大脑皮层和脑干bFGF和FGFR1蛋白表达开始显著增加,1～3d达高峰,7d时已有所下降;海马冲击后3h即开始增加,1d达峰值,此后逐渐下降,7d时恢复正常。结论脑损伤可诱导bFGF/FGFR1的表达,提示机体对脑损伤存在自身保护机制,其表达的时序性改变可望用于法医学脑损伤时间推断。

外源性碱性成纤维细胞生长因子对肠缺血-再灌注大鼠肝脏内源性碱性成纤维细胞生长因子及其受体表达的影响

目的：通过观察外源性碱性成纤维细胞生长因子（ｂＦＧＦ）对缺血 再灌注大鼠肝脏内源性ｂＦＧＦ及碱性成纤维细胞生长因子受体（ＦＧＦＲ１）表达水平的影响，探讨ｂＦＧＦ调控内脏损伤修复的分子机制。方法：采用大鼠肠系膜上动脉夹闭模型，将动物随机分为假手术组、缺血即刻组、外源性ｂＦＧＦ治疗组及未治疗的再灌注６、２４ 和４８小时组。ｂＦＧＦ和ＦＧＦＲ１ 的表达水平采用免疫组织化学ＳＰ方法测定。结果：缺血 再灌注损伤后内源性ｂＦＧＦ和ＦＧＦＲ１ 表达水平均明显提高，分别在再灌注６小时和２４ 小时达峰值，４８小时后下降。应用外源性ｂＦＧＦ治疗后，在组织学损伤得到明显改善的同时，ｂＦＧＦ表达水平也较非治疗组明显提高，而ＦＧＦＲ１ 的表达水平无变化。结论：缺血 再灌注损伤诱导了内源性ｂＦＧＦ和ＦＧＦＲ１ 的表达，而外源性ｂＦＧＦ可能通过上调内源性ｂＦＧＦ的表达或其自身与ＦＧＦＲ１ 结合，调控肝损伤后的组织修复。

碱性成纤维细胞生长因子及其受体FGFR1在脉络膜新生血管中的表达

目的 研究碱性成纤维细胞生长因子 (bFGF)及其受体FGFR1在氪激光诱导的棕色挪威 (BN)大鼠脉络膜新生血管 (CNV)形成中的作用机制。方法 应用氪激光 ( 64 7nm ,3 60mW ,5 0 μm ,0 .0 5s)对 3 0只雄性BN大鼠实验眼进行视网膜光凝 ,分别于光凝后 3、7、14、2 1、2 8和 5 6d摘除眼球进行原位杂交检测bFGFmRNA ,免疫组织化学检测bFGF和FGFR1。结果 光凝 3d后 ,光凝区视网膜内bFGFmRNA和FGFR1蛋白表达水平逐渐下降 (P <0 .0 1)。 7d后视网膜下出现bFGFmRNA和FGFR1染色阳性的CNV ,此后其阳性染色面积及密度逐渐增加 (P <0 .0 1)。结论 bFGF和FGFR1通过自分泌和旁分泌途径在新生血管形成部位结合 ,引起FGFR1自磷酸化 。

bFGF、FGF受体I在HEp-2喉癌和MGE803胃癌细胞株中表达的检测

目的 通过对碱性成纤维细胞生长因子 (basicfibroblastgrowthfactor ,bFGF) ,成纤维细胞生长因子受体 1(fibroblastgrowthfactorreceptor 1,FGFR 1)的检测 ,揭示两者在体内外的表达以及与肿瘤形成的关系。 方法 采用免疫组织化学的检测方法 ,检测了体外培养的HEP 2喉癌细胞和MGE80 3胃癌细胞以及由两者在裸鼠皮下形成的实体瘤组织中bFGF和FGFR 1的表达情况。 结果 在体外培养的这两种肿瘤细胞中bFGF的阳性染色存在于整个细胞。FGFR 1的染色主要存在于细胞核。在两种肿瘤细胞形成的实体瘤组织中bFGF和FGFR 1阳性染色细胞主要是围绕于坏死区的肿瘤细胞。 结论 此两种肿瘤细胞在体内外均能表达bFGF和FGFR 1。bFGF与其高亲和力受体FGFR 1结合后进入细胞核 ,并在细胞核内发挥其生物功能 ,参与了肿瘤组织的形成和发展。