PGE2和NF-кB信号途径在骨再生中的相互作用

目的 本研究旨在利用MC3T3-E1成骨细胞株与大鼠骨折模型来研究骨折愈合过程中PGE2和NF-кB信号途径的相互作用.方法 利用PGE2与NF-кB抑制剂BAY 11-7082处理MC3T3-E1成骨细胞和大鼠骨折模型,采用碱性磷酸酶活性测定、Western blot分析、EMSA分析以及ELISA测定等研究手段,研究PGE2、NF-кB、BMP-7、Id2以及SOD2在骨再生中的作用.结果 利用10 μmol/l PGE2处理MC3T3-E1细胞10 min,30 min和2h后,能够显著地促进成骨细胞增殖与分化,当细胞用5μmol/L BAY 11-7082处理后,PGE2诱导作用受到抑制,表明PGE2增加ALP的表达是通过NF-kB途径来介导.局部注射NF-kB抑制剂后PGE2的生物合成明显减少;此外,抑制骨折部位ALP的活性,在骨折的损伤修复过程中,NF-кB、BMP-7以及SOD2的表达均明显上升,而Id2的表达明显下降；加入NF-кB活性抑制剂后,BMP-7与Id2的表达恢复到正常水平,而SOD2的表达没有改变. 结论 PGE2能够同时通过抑制Id2细胞因子和激活NF-кB信号途径诱导成骨细胞分化.     

尤瑞克林治疗急性前循环脑梗死的近期疗效和安全性研究

目的 评价尤瑞克林治疗急性前循环脑梗死的近期疗效和安全性.方法 采用随机、单盲、对照设计,纳入珠江医院神经内科自2006年10月至2009年4月收治的61例急性前循环脑梗死患者,并按随机数字表法分为尤瑞克林组(31例)和对照组(30例).两组患者根据病情给予相同的基础治疗,尤瑞克林组存此基础上予以每天0.15 PNA单位尤瑞克林(以100mL生理盐水稀释,30～40滴/min静脉滴注,每天1次,连续14 d).在治疗前及治疗后第21天分别观察两组患者神经功能缺损程度(NIHSS评分)及日常生活能力(mRS评分),并进行血尿常规、肝肾功能、血糖、血脂及心电图等检查,监测血压和脉率,必要时复查头颅CT,观察药物相关的出血性事件及不良反应.结果 与对照组相比,尤瑞克林能明显改善患者NIHSS评分和提高mRS评分,差异有统计学意义(P=0.022,P=0.032).依据平均秩次(尤瑞克林组23.86,对照组35.93)判断,尤瑞克林组疗效优于对照组.除尤瑞克林组2例有哮喘病史患者因治疗期间诱发哮喘发作而退出试验外,其他患者未见不良反应.尤瑞克林组用药前后血尿常规、肝肾功能、血糖、血脂及心电图等检查无异常变化,用药后头颅CT检查未见药物相关的出血性事件.结论 应用尤瑞克林治疗急性前循环脑梗死患者安全、有效,能显著改善患者神经功能缺损症状和提高日常生活能力.

Abstract：

Objective To evaluate the short-term therapeutic efficacy and safety of kallikrein in patients with acute anterior circulation cerebral infarction. Methods Sixty-one patients with anterior circulation cerebral infarction, admitted to our hospital from October 2006 to April 2009, were enrolled in the randomized single-blind control trail. These patients were assigned to kallikrein treatment group (n=31) and control group (n=30). They were both treated by identical basis therapy, such as antiplatelet,dilute blood viscosity, neurotrophy therapy and symptomatic treatment. The patients in the treatment group were treated by intravenous infusion administration of 0.15 PNA kallikrein diluted in 100 mL 0.9% saline at 30-40 drops /min once daily for 14 consecutive days. On the pretherapy and 21st post-treatment day, the National Institutes of Health Stroke Scale (NIHSS), activity of daily living (ADL) of modified Rankin Scale (mRS) in these patients were performed;blood routine examinations and urinalysis,hepatorenal function, levels of blood glucose and lipid, and ECG were assessed;blood pressure and pulse rate were monitored. CT scan was employed for ICH if necessary. Drug relative hemorrhage and adverse drug reaction (ADR) were recorded in detail. Results As compared with those in the control group,significantly reduced NIHSS scores and obviously improved ADL scores in the kallikrein treatment group were noted (P=0.022, P=0.032, respectively). According to the mean rank (kallikrein treatment group:23.86, control group: 35.93), the efficacy in the treatment group was better than that in the control group.Except that asthmatic attack happened to 2 patients (having the history of asthma) during treatment period, no other ADRs were noted in all the patients. No abnormal changes of blood routine examinations, urinalysis, hepatorenal function, levels of blood glucose and lipid, and ECG and head CT features in the kallikrein treatment group were detected before and after the treatment;no drug relative hemorrhage was noted either. Conclusion Kallikrein is safe and effective in treating patients with acute anterior circulation cerebral infarction, through reducing the neurologic function impairment and improving ADL.     

PGE2 和 NF-κB信号途径在骨再生中的相互作用

目的　本研究旨在利用MC3T3-E1 成骨细胞株与大鼠骨折模型来研究骨折愈合过程中PGE2和NF-κB信号途径的相互作用。 方法　利用PGE2与NF-κB 抑制剂 BAY 11-7082处理MC3T3-E1成骨细胞和大鼠骨折模型，采用碱性磷酸酶活性测定、Western blot 分析、EMSA分析以及ELISA测定等研究手段，研究PGE2、NF-κB、BMP-7、 Id2以及SOD2在骨再生中的作用。 结果　利用10 μmol/l PGE2处理MC3T3-E1细胞10 min, 30 min 和2h后，能够显著地促进成骨细胞增殖与分化，当细胞用5 μmol/L BAY 11-7082处理后，PGE2诱导作用受到抑制，表明 PGE2 增加ALP的表达是通过NF-κB 途径来介导。局部注射NF-κB 抑制剂后 PGE2 的生物合成明显减少；此外，抑制骨折部位ALP的活性，在骨折的损伤修复过程中，NF-κB、BMP-7以及SOD2 的表达均明显上升，而Id2的表达明显下降；加入NF-κB活性抑制剂后，BMP-7与Id2的表达恢复到正常水平，而SOD2的表达没有改变。　结论 　PGE2能够同时通过抑制Id2细胞因子和激活NF-κB信号途径诱导成骨细胞分化。     

miRs在力学拉伸促进成肌细胞增殖过程中的作用

目的　探讨3种miRs在力学拉伸促进C2C12成肌细胞增殖过程中的作用。  方法　周期性拉伸的各种力学条件通过 BioFlex 加载系统实现。 采用CCK-8检测不同拉伸频率对成肌细胞增殖的影响。对促增殖拉伸组和对照组进行高通量测序, 反转录定量 PCR(qRT-PCR) 验证高通量基因测序结果,并进行生物信息学分析。   结果　 0.125 Hz拉伸组明显促进C2C12成肌细胞增殖（P<0.05）,而0.25 Hz 和0.5 Hz相比于对照组的差异无统计学意义;高通量测序分析表明,11种miRs表达于对照组和0.125 Hz拉伸组,其中差异有统计学意义的为3种：mir-44,mir-36,mir-20;qRT-PCR证实这3种miRs的表达改变与测序结果一致;这3种miRs参与了多个信号通路的调控。  结论　高通量基因测序和生物信息学分析表明3种miRs在应力诱导的C2C12成肌细胞增殖过程中有重要作用。