生长反应因子与大鼠颈动脉损伤后内膜增生

背景：经皮冠状动脉介入治疗后再狭窄仍是影响介入治疗远期疗效的严重的临床问题。 目的：在大鼠颈动脉球囊损伤模型中,探讨早期生长反应因子诱骗寡脱氧核苷酸对损伤后的血管内膜的影响,并初步探讨其分子机制。 方法：利用2F Fogarty导管损伤Wistar大鼠颈动脉,构建大鼠球囊损伤模型,在转染试剂Fugene 6介导下经血管腔内转染生长反应因子诱骗寡脱氧核苷酸,苏木精-伊红染色法观察血管内膜增生情况,免疫组化法检测Cyclin D1,观察其表达情况。 结果与结论：早期生长反应因子诱骗寡脱氧核苷酸可以显著抑制大鼠颈动脉球囊损伤后血管内膜增生,同时也可以下调大鼠颈动脉球囊损伤后表达显著增加的Cyclin D1。说明生长反应因子诱骗寡脱氧核苷酸可能通过抑制Cyclin D1的表达,使细胞周期停滞,从而抑制损伤后的大鼠颈动脉内膜的增生。     

乙醇性脂肪肝模型大鼠早期生长反应因子1表达及水飞蓟素的干预

背景：促炎性转录因子以及炎性因子在乙醇性肝病的发生中起着重要作用,而早期生长反应因子1正是炎症启动的关键因子之一。 目的：观察并分析水飞蓟素对乙醇性脂肪肝模型大鼠早期生长反应因子1的影响。 方法：将大鼠采用高脂饮食联合乙醇灌胃方式建立脂肪肝动物模型,每次灌胃后分别给予水飞蓟素高、低剂量(200,100 mg/kg)干预,并设正常组进行对照,共灌胃8周。 结果与结论：血清学指标检测和苏木精-伊红染色结果显示,与模型组相比,水飞蓟素高剂量组大鼠体质量增高(P < 0.05),血清谷草转氨酶、谷丙转氨酶活性、肝组织早期生长反应因子1和肿瘤坏死因子α的表达降低(P < 0.05),病理分级结果均占优(P < 0.01)。结果证实,高剂量水飞蓟素能有效保护大鼠肝功能,减少肝功能损害的发生,可能与水飞蓟素抑制大鼠体内早期生长反应因子1,从而减少肿瘤坏死因子α的形成有关,但具体机制尚待进一步研究。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

电镜下观察动脉粥样硬化血管损伤模型大鼠的血管超微结构

BACKGROUND: Animal models of vascular restenosis used to be established in the normal vessels, and study on the healing results limits in the normal artery, not atherosclerosis; thereby, the model cannot accurately simulate the pathological process after percutaneous transluminal coronary angioplasty. OBJECTIVE: To establish the common carotid catheter injury model in atherosclerosis rats and to study the pathogenesis of restenosis.  METHODS:The balloon catheter injury was performed on the left common carotid artery of atherosclerosis rats with 2F balloon catheter. The dynamic changes of neointimal and media hyperplasia were observed at different time points after surgery. Meanwhile, the ultrastructure of arterial wall was observed using transmission electron microscope.  RESULTS AND CONCLUSION:The neointima formed at 7 days, and reached a peak at 3 months, vascular lumen was seriously narrow, and abundant smooth muscle proliferation could be found in the damaged artery wall. The smooth muscle cells switched from contractile type to synthetic type at the beginning after injury, and most of cells returned to contractile type finally. These findings indicate that 2.0 balloon catheter can successfully establish the carotid injury model in atherosclerosis rats; neointima hyperplasia results in lumen stenosis after injury; furthermore, phenotype transformation, proliferation, and migration of smooth muscle cells play an important role in the process of neointima hyperplasia. 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

血小板反应蛋白1在纤维化模型大鼠肾组织中的表达

BACKGROUND:Thrombospondin-1 is an important endogenous activator of transforming growth factor beta 1 in this experimental inflammatory kidney disease model. Transforming growth factor beta 1 is considered the major cytokine that causes tissue fibrosis in many different inflammatory disease processes, in particular in renal disease. OBJECTIVE:To investigate the expression of thrombospondin-1 on renal fibrosis in rats. METHODS:Healthy male Sprague-Dawley rats were randomly divided into sham surgery group and model group. In the model group, right ureters of rats were ligated to construct models of renal fibrosis. 3 weeks after surgery, blood and urine were obtained weekly. Enzyme linked immunosorbent assay and Bradford method were used to detect the contents of serum creatinine, blood urea nitrogen and urinary protein. After rats were sacrificed, kidneys were fixed. Western blot assay was utilized to identify the expression of vascular endothelial growth factor, transforming growth factor beta 1 and thrombospondin-1 protein. Hematoxylin-eosin staining was applied to detect the changes in pathological structure of the kidney after surgery. RESULTS AND CONCLUSION: (1) One week after model induction, urinary protein, serum creatinine and urea nitrogen levels were significantly higher in the model group than in the sham surgery group (P < 0.05). Three weeks later, the difference in each index was significant (P < 0.01), which showed that the injury of the kidney was aggravated. (2) Transforming growth factor beta 1 protein and thrombospondin-1 expression was significantly higher in the model group than in the sham surgery group, but vascular endothelial growth factor protein expression was significantly lower in the model group than in the sham surgery group. (3) Hematoxylin-eosin staining results demonstrated that severe pathological changes of renal tissue in rats were detected after ligation of renal tubule. (4) These results confirmed that thrombospondin-1 expression increased in renal tissue, and its expression was strongly associated with vascular endothelial growth factor protein and transforming growth factor beta 1, which may play an important role in the renal fibrosis.     

早期应用生长反应因子1小干扰RNA可抑制烟草烟雾刺激大鼠主动脉平滑肌细胞白细胞介素1β mRNA的表达

背景：研究表明,在动脉粥样硬化的血管壁细胞中白细胞介素1β表达水平升高。 目的：观察早期生长反应因子1的小干扰RNA对烟草烟雾提取物刺激大鼠主动脉平滑肌细胞中白细胞介素1β mRNA表达的影响。 方法：体外培养大鼠主动脉平滑肌细胞,用不同体积分数(0%,5%,10%,20%和40%)烟草烟雾提取物刺激细胞,筛选最佳体积分数烟草烟雾提取物干预细胞0,8,16和24 h,以确定最佳干预时间,最后用生长反应因子1小干扰RNA以沉默细胞中生长反应因子1的表达。  结果与结论：RT-PCR结果显示,烟草烟雾提取物可诱导大鼠主动脉平滑肌细胞白细胞介素1β mRNA的表达,且有时间和浓度依赖性,烟草烟雾提取物最佳干预时间为8 h,最佳干预体积分数为10%。将生长反应因子1小干扰RNA转染10%烟草烟雾提取物刺激的细胞后8 h,白细胞介素1β mRNA表达明显减少(P < 0.05)。证实早期应用生长反应因子1小干扰RNA可以抑制烟草烟雾提取物诱导的大鼠主动脉平滑肌细胞中白细胞介素1β mRNA的表达。     

Notch1和Bmi-1蛋白在肺癌组织中的表达及意义

BACKGROUND: Studies have found that Notch pathway and Bmi-1 gene both have the ability to regulate stem cell self-renew. Functional dysfunction of the both may have a great relationship with tumorigenesis. OBJECTIVE: To investigate the expression and clinical significance of Notch1 and Bmi-1 protein in lung tissue. METHODS: Eighty-seven lung cancer tissue samples (lung cancer group) and forty pathologically confirmed normal lung tissue samples (normal group) were obtained from related surgeries and included as research objects. The protein expression of Notch1 and Bmi-1 in specimens of these two groups was measured by immunohistochemistry SP method. The relationship between Notch1 and Bmi-1 protein expression and clinicopathological features of lung cancer patients was analyzed. RESULTS AND CONCLUSION: The positive rate of Notch1, Bmi-1 protein expression was respectively 61% and 47%, which was significantly higher in the lung cancer group than that in the normal group (P < 0.05). In the lung cancer group, Notch1 protein expression was significantly positively correlated with Bmi-1 protein expression (r=0.567, P < 0.001). There were no significant differences in Notch1 and Bmi-1 protein expression rates between different genders and different pathological types of patients (P < 0.05). The Notch1 and Bmi-1 protein positive expression rates in poorly-differentiated, TNM stage III-IV lung cancer patients with lymph node metastasis were significantly higher than those in well- and moderately-differentiated, TNM stage I-II lung cancer patients without lymph node metastasis (P < 0.05). These results demonstrate that Notch1 and Bmi-1 protein may have certain relationship with the occurrence and development of lung cancer.       

转铁蛋白受体1与早期生长反应因子4在宫颈癌组织中的表达及其临床意义

为研究转铁蛋白受体1(transferrin receptor type 1,TfR1)与早期生长反应因子4(early growth response protein 4, EGR4)在宫颈癌(uterine cervical carcinoma, UCC)组织中的表达水平,并分析其与UCC临床病理分期的相关性,选取2012年3月至2018年5月于武汉市第四医院就诊的慢性宫颈炎患者33例、宫颈上皮内瘤变(cervical intraepithelial neoplasia, CIN)患者78例、宫颈鳞癌患者63例。采集宫颈炎症和癌变组织,采用免疫组织化学法检测组织中TfR1与EGR4的表达水平,并分析两者之间的相关性及其与宫颈鳞癌临床病理分期的关系。结果显示,TfR1与EGR4在慢性宫颈炎、CIN及宫颈鳞癌组织中均有表达,其中在慢性宫颈炎组织中的表达水平最低(分别为6.1%、9.1%),而在CIN组织中的表达水平随分期的增加而上升,在宫颈鳞癌组织中的表达水平最高(分别为74.6%、57.1%)。相关性分析显示,TfR1与EGR4的表达呈正相关(r_s=0.695,P0.001),而两者表达水平均与患者年龄、肿瘤大小无关;TfR1的表达水平在不同国际肿瘤学会和国际妇产科协会(the International Federation of Gynecology and Obstetrics, FIGO)分期和分化程度患者中存在差异(χ~2=16.937,P0.001;χ~2=8.051,P=0.018),EGR4的表达水平则仅在不同FIGO分期患者中不同(χ~2=8.974,P=0.003)。提示在宫颈鳞癌的发生、发展过程中TfR1与EGR4起着重要作用,其中TfR1的表达随着肿瘤细胞分化程度的降低、FIGO分期的增加而上升,EGR4的表达水平则仅随FIGO分期的增加而上升。     

构建颈动脉损伤模型大鼠早期生长反应因子1及组织因子的表达（英文）

背景:脱氧核酶ED5可通过特异性抑制早期生长反应因子1的表达来阻遏下游靶基因的表达。目的:构建颈动脉损伤模型大鼠,观察早期生长反应因子1的脱氧核酶ED5对大鼠颈动脉损伤后血浆组织因子水平的影响及防治血管内膜增生的机制。方法:实验采用左颈总动脉内膜剥脱构建颈动脉球囊损伤模型大鼠,分别将ED5,MgC l2和FuG ene6注入大鼠损伤的血管节段内。结果与结论:病理学检查、免疫荧光染色、免疫组织化学染色、ELISA检测结果显示,建模后3,7,14,21 d,与MgC l2组和Fu Gene6组相比,经损伤动脉局部转染ED5后的大鼠血管组织早期生长反应因子1的表达和血浆组织因子的表达水平明显减少(P0.01),且建模后7,14,21 d内膜增生程度明显减轻(P0.01)。结果证实,早期生长反应因子1特异脱氧核酶ED5可能通过抑制组织因子的表达,从而抑制损伤颈动脉内膜的增生。     

早期生长反应基因-１在急性胰腺炎大鼠肝组织的表达

目的： 观察早期生长反应基因-１(Egr-1)在大鼠不同程度急性胰腺炎（AP）及AP发病后不同时间在肝组织的表达，并研究EGR-1与AP肝脏损害的关系。方法: 先将24只雄性Wistar大鼠随机均分为4组，即A、B、C、D 4组，分别于胆总管内逆行注入生理盐水或不同浓度牛磺胆酸钠溶液，3 h后处死动物，留取血清、肝脏及胰腺组织。另将30只雄性Wistar大鼠随机均分为５组，即E、F、G、H、I组，5%牛磺胆酸钠溶液（0.75 mL/kg）胆管内逆行注射，分别于注射后1 h、3 h、6 h、12 h、24 h处死动物同上留取标本。检测血清AST、LDH、TNF-α、IL-1β水平，对胰腺组织病理评分，并对肝组织进行EGR-1免疫组化染色。结果: (1)通过注射不同浓度牛磺胆酸钠溶液，成功地复制出不同严重程度的AP动物模型，A、B、C、D 4组动物胰腺病理评分、炎性细胞因子水平、AST及LDH水平均随着牛磺胆酸钠浓度的升高而逐渐上升；(2)肝组织EGR-1免疫组化染色显示，在不同程度AP组，EGR-1表达量随AP病情加重而逐渐增加，并与反映AP病情各指标如肝实质酶、炎性细胞因子浓度、胰腺病理评分均呈显著正相关，且表达部位也有所不同。EGR-1在AP发病后不同时间肝组织的表达，具有极明显的细胞种类与部位的差异。在观察时间内，以发病后3 h表达量最高。结论: EGR-1可能与AP时伴发的肝脏损害严重程度有关，其机制可能与其介导的炎性细胞因子生成有关。     

组织因子途径抑制物基因局部转染对兔颈总动脉损伤后内膜增生及P53表达的影响

目的研究组织因子途径抑制物(TFPI)基因局部转染对兔颈总动脉损伤处内膜增生及P53表达的影响。方法36只新西兰纯种雄性大白兔颈总动脉损伤后随机分生理盐水组?复制缺陷型腺病毒(AdLacz)组和包载TFPI目的基因复制缺陷型腺病毒(AdTFPI)组。每组12只。术后14d处死动物,取损伤血管进行检测分析。免疫组化染色观察TFPI在转染局部的表达成功;颈总动脉损伤处抽提总RNA,半定量逆转录多聚酶链式反应(RT-PCR)测定P53mRNA表达;同时对颈总动脉病变最明显的取材标本进行HE染色,光学显微镜下观察血管内膜增生,以计算机图像分析系统分析血管内膜?中膜面积和腔面积。结果AdTFPI组家兔的颈总动脉损伤处血管内膜的增生显著受抑制?内膜/中膜面积比值下降;生理盐水组?AdLacz组和AdTFPI组P53mRNA的相对值分别为1.31±0.14、1.27±0.11和4.21±0.87,P53在AdTFPI组表达增强,与前两者相比有显著差异性。结论TFPI基因局部转染显著抑制颈总动脉损伤处血管内膜的增生并增强P53表达。     

颈内动脉虹吸部血流动力学模拟与影响因素

背景：颈内动脉虹吸部走行弯曲、周围结构复杂,解剖学、影像学测量研究较多,并成为相关领域的研究热点,但目前对颈内动脉虹吸部血流动力学的相关研究报道较少,利用有限元分析技术,为相关动力学研究提供了基础。目的：明确颈内动脉虹吸部正常及狭窄血液动力学特点,探讨血流动力学的影响因素。方法：利用64排螺旋CT扫描获得DICOM数据实现颈内动脉虹吸部有限元建模,分别在Mimics 10.01软件上进行三维模型的实体构建,用ANSYS 13.0 CFX软件模拟仿真人类颈内动脉虹吸部正常及狭窄后血流,观察正常血流及狭窄后血流动力学的改变,分析其特点与差异。结果与结论：颈内动脉虹吸部正常血流在弯曲的虹吸部呈层流状态,但经过两个折角时血流发生旋动与湍流。血流经折角内弯区较快,外弯区较慢,速度越慢湍流越明显;折角处剪切力较小,同时折角外弯区剪切力较内弯区小。动脉狭窄后血流经狭窄区速度加快,狭窄下游形成湍流及低剪切力区;随狭窄程度增大,湍流、低剪切力区域扩大,中央性狭窄比偏心性狭窄影响大。结果证实,颈内动脉虹吸部弯曲、管腔狭窄直接影响湍流及低剪切力区形成,以外弯区及中央性狭窄影响明显。中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

股动脉血栓模型兔溶栓前后血管弹性功能变化

BACKGROUND:Ultrasonic technology has been extensively applied to evaluate the vascular elasticity changes, but thrombosis and elasticity changes of the proximal thrombus (the artery of proximal heart, 1 cm distance from the thrombosis) after revascularization are rarely reported. OBJECTIVE: To evaluate the elasticity changes of the unilateral femoral artery of proximal thrombus in rabbits before and after thrombolysis utilizing ultrasonic technology. METHODS: Models of unilateral femoral artery thrombosis were successfully prepared in 30 New Zealand white rabbits, and then given thrombolytic therapy by targeted microbubbles carrying urokinase under low- frequency ultrasound. The arterial expansion coefficient, compliance coefficient, elastic coefficient, stiffness, pulse wave velocity, augment index, as well as systolic radial strain and radial strain rate before and after thrombosis and after thrombolysis were determined, respectively. REAULTS AND CONCLUSION: Compared with before thrombosis, the arterial elastic coefficient, stiffness, pulse wave velocity and augment index were significantly increased in contrast to the significantly decreased arterial expansion coefficient, compliance coefficient, systolic radial strain and radial strain rate after thrombosis (P < 0.05). Thrombolytic therapy significantly increased the arterial expansion coefficient, compliance coefficient, systolic radial strain and radial strain rate and eliminated the arterial elastic coefficient, stiffness, pulse wave velocity and augment index (P < 0.05). In addition, the arterial elastic coefficient, stiffness, pulse wave velocity and augment index after complete revascularization were significantly higher than those before thrombosis (P < 0.05), but there were no significant differences in the arterial expansion coefficient, compliance coefficient, systolic radial strain and radial strain rate between two groups. In conclusion, thrombosis contributes to the increased arterial stiffness and elasticity dysfunction, and thrombolytic therapy can, but not completely, improve artery elastic function. 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

建立一种新型凝血因子Ⅴ基因突变小鼠模型：突变小鼠无显著骨组织变化

BACKGROUND: Blood coagulation factor V gene mutation in non-traumatic femoral head necrosis has been shown to have an higher incidence than that in healthy and secondary non-traumatic femoral head necrosis, and the incidence of thrombosis is positively related. Inactivated blood coagulation factor V can accelerate the activation of prothrombin and the generation of thrombin. Mutations at arg-306, arg-506 and arg-679 will result in the blood clots and hypercoagulable state. Here, this study is designed to investigate the influence of R506Q/R679Q on osteonecrosis. OBJECTIVE: To establish the mouse model of mutations of Gln506Arg and Gln679Arg in coagulation Factor V (Factor VR506Q/R679Q). METHODS: Factor VR506Q/R679Q point mutation target vector was constructed by molecular cloning technology, the linearization vector was transfected into embryonic stem cells, and then G418-resistant cells were screened and used for microinjection. The target blastocysts were transplanted to the fallopian tube of estrus mice to obtain the Chimera mice carrying bilateral LoxP gene, followed by mated with CMV-cre transgenic mice, and then the mice with Factor VR506Q/R679Q point mutations were obtained. After genotype identification by PCR, hematoxylin-eosin staining results and percentage of empty lacunae were compared between the mutant and wild-type mice, and rat bone tissue and bone mass were analyzed. RESULTS AND CONCLUSION: There were no obvious abnormalities in the embryonic and postnatal development, percentage of empty lacunae and bone mass of Factor VR506Q/R679Q point mutation mice when compared with the wild-type mice. These results suggest that the mouse model with Factor VR506Q/R679Q point mutation is established successfully, but there is no significant change in the bone tissue. The following research should focus on the effect of external stimulus on the incidence of osteonecrosis in a mutant mouse. 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

兔股动脉粥样硬化斑块模型中TF及TFPI的变化

目的： 观察兔股动脉粥样硬化斑块发展过程中斑块内组织因子（TF）及组织因子途经抑制物-1（TFPI-1）、组织因子途经抑制物-2（TFPI-2）的变化。方法： 新西兰雄兔通过高脂饲养合并股动脉球囊损伤建立动脉粥样硬化斑块模型。在建模8周、10周和12周，分别截取球囊损伤处股动脉标本，检测斑块组织内TF、TFPI-1和TFPI-2的蛋白表达；并测定斑块内TF、TFPI-1和TFPI-2的mRNA水平。结果： 自8周、10周到12周，血管斑块中TF、TFPI-1和TFPI-2的观测区域内阳性染色面积均逐渐增加。自8周、10周到12周，血管斑块中TF的mRNA水平和TFPI-1的mRNA水平均逐渐增加；TFPI-2mRNA表现为前期无明显变化，12周时显著下调。结论： 在兔股动脉粥样硬化斑块的形成过程中，随着斑块内TF基因及蛋白表达的增加,TFPI-1和TFPI-2反应性表达增加，但其表达水平未能完全抑制斑块的进展。     

大鼠C-sis基因克隆及其真核表达载体的构建

BACKGROUND: C-sis proto-oncogene can promote tissue repair by inducing cell proliferation and inhibiting cell apoptosis. Therefore, C-sis may play a positive role in the repair of damaged liver tissue and the treatment of fulminant hepatic failure. OBJECTIVE: To construct pcDNA3.1/C-sis eukaryotic expression vector and detect its expression in BRL cells (the normal liver cells of rats) and rat liver cells in vivo. METHODS: The full-length coding sequence of C-sis gene was cloned through real time-PCR. pcDNA3.1/C-sis eukaryotic expression vector was constructed and sequenced, followed by transfected into BRL cells using liposome and injected into the rat liver via tail vein. Finally, its expression in BRL cells and rat liver cells in vivo was identified by fluorescence quantitative PCR and western blotting. RESULTS AND CONCLUSION: (1) The full length of encoding region of C-sis gene was successfully cloned. Sequencing proved that pcDNA3. 1/C-sis recombinant eukaryotic expression vector was constructed successfully. (2) The expression of C-sis was increased after transfected into BRL cells and rat liver. (3) These results provide basis for the subsequent study of the effect of C-sis gene on fulminant hepatic failure in rats. 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

血管内皮生长因子和骨形态发生蛋白在骨组织工程中的作用

背景：在临床中由于骨质疏松性骨折、创伤、先天性骨发育不良、进行性骨骼紊乱引起的大段结构性骨缺损非常常见,组织工程骨为骨缺损的修复提供了新希望。骨组织工程研究中关于生长因子的研究较多,已取得了一些成果,如何在时间上控制各种不同生物活性的生长因子是研究热点。目的：综述血管内皮生长因子和骨形态发生蛋白在血管化组织工程骨中的研究进展。方法：由第一作者用计算机检索中国期刊全文数据库(CNKI：1990至2015年)Medline(1990至2015年)数据库,检索词分别为“成骨因子、成血管因子、组织工程骨、骨修复、血管化、血管内皮生长因子、骨形态发生蛋白、序贯释放、种子细胞、细胞支架”和“osteogenic factors,angiogenic factors,tissue engineering bone,bone repair,vascularization,VEGF,BMPs,sequential release,seed cells,cytoskeleton”,语言分别设定为中文和英文。检索有关血管内皮生长因子和骨形态发生蛋白在骨修复作用中的研究,并总结作用机制及研究方向。结果与结论：共检索到313篇文献,按纳入及排除标准筛选后,纳入文章87篇。结果表明,骨缺损的重建伴随着多种不同的生物活性分子,各自具有不同的潜能和效率。血管和成骨是骨修复两个最为重要的过程,成骨生长因子在维持骨骼结构和骨形成中发挥重要的作用,而成血管生长因子可以为组织的生长、分化和功能化提供氧气和营养物质,双因子或多因子联合作用是目前但骨组织工程中的一个发展方向,成骨与成血管生物因子比单独使用其中一种具有更好的成骨效果,但是控制外源性成骨与成血管生物因子的释放剂量是在治疗过程中的关键研究问题。中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

成纤维细胞生长因子修饰骨髓间充质干细胞可促进颅脑损伤后功能的恢复

背景：骨髓间充质干细胞虽然能促进神经再生,但因治疗方式局限,并未取得较好的疗效。应用单纯的骨髓间充质干细胞移植治疗脑损伤还远不能达到治疗和改善病情的目的。 目的：探讨成纤维细胞生长因子修饰的骨髓间充质干细胞对颅脑损伤后功能恢复及胶质纤维酸性蛋白表达的影响。 方法：采用液压冲击法建立SD大鼠颅脑创伤模型,建模后随机分为对照组(颅脑损伤组)、骨髓间充质干细胞组及成纤维细胞生长因子-骨髓间充质干细胞组。体外分离、培养骨髓间充质干细胞,利用腺病毒载体介导成纤维细胞生长因子基因转染入骨髓间充质干细胞。采用Western-Blot法检测成纤维细胞生长因子基因转染及胶质纤维酸性蛋白的表达情况;应用免疫组化检测BrdU标记的骨髓间充质干细胞在脑内的分布及数量;利用Longa评分法于移植后1 d、3 d、1周、2周对大鼠进行神经功能学评分;TUNEL法检测脑组织细胞的凋亡情况。 结果与结论：Western-Blot结果显示,成纤维细胞生长因子基因成功转入腺病毒载体,并且能够在骨髓间充质干细胞中表达,且胶质纤维酸性蛋白在成纤维细胞生长因子-骨髓间充质干细胞组的表达明显高于其他两组(P < 0.05)。BrdU标记的骨髓间充质干细胞在成纤维细胞生长因子-骨髓间充质干细胞组脑组织中的表达明显高于其他两组(P < 0.05)。移植后2周,成纤维细胞生长因子-骨髓间充质干细胞组大鼠的神经功能缺损Longa评分明显低于其他两组(P < 0.05)。TUNEL检测到的凋亡细胞数在成纤维细胞生长因子-骨髓间充质干细胞组明显少于其他两组(P < 0.05)。提示成纤维细胞生长因子修饰的骨髓间充质干细胞移植能够减轻颅脑损伤模型大鼠的神经功能损伤程度,促进神经功能恢复,效果优于骨髓间充质干细胞单独移植治疗。 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

胰岛素样生长因子Ⅰ转染对脂肪干细胞TWEAK/Fn14信号通路的影响

背景：胰岛素样生长因子Ⅰ具有诱导间充质干细胞向软骨细胞分化的能力,通过基因转染的方式将胰岛素生长因子Ⅰ转染入脂肪干细胞或许能够更好的促进脂肪干细胞向软骨细胞分化。 目的：探讨胰岛素样生长因子Ⅰ基因对脂肪间充质干细胞体外定向成软骨分化能力以及对TWEAK/Fn14信号通路的影响。 方法：构建慢病毒载体pLVX-IGF-I-IRES-ZsGreenl基因并转染第3代人脂肪间充质干细胞,诱导细胞向软骨分化。同时将pLVX-IRES-ZsGreenl转染的脂肪间充质干细胞设为绿色荧光蛋白/脂肪间充质干细胞组,单纯脂肪间充质干细胞设为对照组。 结果与结论：与绿色荧光蛋白/脂肪间充质干细胞组和对照组相比,胰岛素样生长因子Ⅰ/脂肪间充质干细胞组细胞中TWEAK mRNA表达水平降低,而胰岛素样生长因子Ⅰ,Col2al和Sox9 mRNA的表达水平增加,Col2a1表达水平增加,基质金属蛋白酶3以及TWEAK的表达降低。提示pLVX-IGF-I-IRES-ZsGreenl慢病毒转染脂肪间充质干细胞后可获得胰岛素样生长因子Ⅰ的高效表达,且能下调细胞TWEAK基因及蛋白表达,可促进体外培养的脂肪间充质干细胞转化为软骨细胞。 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

胰岛素样生长因子在正畸牙牙周组织改建中的作用

背景：正畸牙牙周组织改建主要是牙槽骨的改建。胰岛素样生长因子是牙周组织改建的重要因子,它在细胞的增殖、分化及个体的生长发育中发挥着重要的促进作用。 目的：综述胰岛素样生长因子在牙周组织改建中的作用。 方法：运用计算机检索PubMed,中国知网以及贵州省数字图书馆等数据库,查阅至今有关胰岛素样生长因子在牙周组织改建中作用的中英文文献。关键词“胰岛素样生长因子;牙周组织;改建;insulin-like growth factor;Periodontal tissue;remodeling”。纳入胰岛素样生长因子与牙周组织改建中作用相关的文献进行归纳分析。 结果与结论：胰岛素样生长因子属于胰岛素家族的一类多肽,对牙周膜中的成骨细胞、成纤维细胞以及诱导间充质细胞等,有促进其细胞迁移、增殖、分化、胶原和基质合成、增强碱性磷酸酶活性及在损伤修复中发挥着重要作用。在正畸治疗中,使用适宜矫治力的同时可适当运用能促进牙周组织改建的胰岛素样生长因子,加快正畸牙齿的移动,缩短患者的矫治时间。  中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程