【摘 要】
：
Aim To observe the protection of Pae on injuried VEC and the improvement of mgration and abnormal proliferation of SMC co-cultured with VECinduced by ox-LDL.To further clarify the relationship between
【机 构】
：
College of Pharmacy Anhui University of Traditional Chinese Medicine,Key Laboratory of Chinese Medic
【出 处】
：
全国中药药理学会联合会学术交流大会
论文部分内容阅读
Aim To observe the protection of Pae on injuried VEC and the improvement of mgration and abnormal proliferation of SMC co-cultured with VECinduced by ox-LDL.To further clarify the relationship between the dysfunction of endothelial cells and SMC proliferation, migration,PI3K-AKT signaling pathway under the conditions of injuried VEC.Methods Establish co-culture system of SMC and VEC.To build VEC damage model, VEC were incubated with ox-LDL.The protection effects of Pae on impaired VEC induced by ox-LDL and the proliferation of SMC were detected by MTT.Transwell chamber was used for testing the role of VEC on SMC migration.The protein levels of VEGF、 PI3K、 AKT、 P-AKT were detected by Western blotting.Besides, the expression of PDGF-B、PCNA were disclosed by Immunohistochemistry.Results Pre-treated VEC with different concentrations of Pae (30,60,120 μ mol · L-1)for 24 h, which could significantly increase the survival rate of VEC;Pae has a maximum inhibition at 120 μ mol.L-1, 240 μ mol.L-1 for 24h;Pae (30,60,120 μ mol.L-1)for 24h could uncommonly reduce the proliferation of SMC co-cultured with impaired VEC induced by ox-LDL, and significantly lower the expression of PCNA of SMC;Pae (30, 60, 120 μ mol· L-1) could obviously inhibit the expression of PDGF-B、 VEGF of VEC;Pae(30, 60, 120μ mol ·L-1)could obviously let down the phosphorylation level of PI3K and AKT induced by ox-LDL.Conclusions It was obviousely that Pae could increase the survival rate of VEC which was decreased by ox-LDL,and that Pae could protect VEC from injuring induced by ox-LDL effectively.And Pae exerts the function of protecting injured VECs, which reduced VEGF, PDGF-B release of VECs and decreased PCNAexpression of VSMCs, prevented PI3K-AKT pathway activation and VSMCs overproliferation and migration.
其他文献
目的：观察生脉注射液改善小鼠脑缺血再灌注损伤的作用,并探讨可能的作用机制,为临床应用于脑中风的防治提供一定实验依据.方法：制备线栓法小鼠大脑中动脉(MCAO)栓塞模型,缺血1h,再灌注24 h后,观察不同剂量生脉注射液(970 mg/kg,485 mg/kg,242.5mg/kg)腹腔注射给药对脑梗塞面积、神经行为学评分等指标的影响,并采用蛋白印迹技术测定脑组织中自噬标记蛋白Beclin1和LC3
目的：观察当归芍药散(DSS)对福尔马林诱导疼痛模型的影响，为进一步探讨当归芍药散的镇痛作用机制提供依据.方法：采用小鼠足底注射5％福尔马林溶液诱导小鼠急性炎性疼痛模型，通过小鼠的缩足次数、舔足时间及yon Frey filaments测定的小鼠机械痛敏来评价DSS的镇痛作用，通过旷场实验和高价十字迷宫，来评价当归芍药散对福尔马林疼痛模型小鼠的自发活动和焦虑/抑郁情绪状态的改善作用.结果：足底注射
目的 探讨梓醇对永久性脑缺血模型急性期脑组织梗死体积、含水量及恢复期早期炎性反应的影响.方法 采用化学刺激法建立局灶性脑缺血(MCAT)模型,检测急性期(24h)神经行为学症状、脑梗死面积和脑含水量；线栓法制作永久性大鼠脑缺血模型(pMCAO),ELISA方法测定缺血侧脑组织IL-6、IL-10和NF-κ Bp65的含量.结果 大鼠MCAT后24 h,梓醇15 mg/kg-60 mg/kg剂量可以
目的 通过部分结扎大鼠肾上腹主动脉建立压力超负荷性心室肥厚模型,来观察liguzinediol对各组大鼠心室重构的影响。方法 用腹主动脉缩窄方法复制大鼠压力超负荷心室重构模型。设假手术组,模型组,liguzinediol高、中、低剂量(20、10、5 mg·kg-1)组及阳性药(卡托普利10 mg·kg-1)组。造模后稳定一周开始灌胃给药,给药8周后测量大鼠心脏动脉收缩压(SBP)、动脉舒张压(D
目的：薯蓣皂苷元作为一种甾体皂苷元,具有显著的抗肿瘤、抗炎、保护心血管等活性,在临床上应用广泛.本实验观察薯蓣皂苷元对肺部炎症的抑制作用,并探讨其可能的作用机制,为药物临床应用提供一定实验依据.方法：采用尾静脉注射脂多糖(LPS) 30mg/kg诱导的小鼠急性肺损伤模型,考察薯蓣皂苷元对肺部水肿等炎症指标的影响,并采用免疫印迹的方法,初步观察薯蓣皂苷元调节NF-κB p50/p65和MAPK/p3
目的：为了探讨中药南蛇藤中活性成分南蛇藤素(celastrol)抗类风湿关节炎(rheumatoid arthritis,RA)滑膜细胞侵袭的机制.方法：体外原代培养人RA滑膜成纤维细胞(fibroblast-like synoviocytes, FLSs),使用MTT和流式细胞仪分析细胞周期方法确定celastrol对RA-FLS的非细胞毒浓度为实验浓度,观察其对(interleukin-17A
目的 研究破血化瘀类中药材斑蝥主要成分斑蝥素的结构衍生物去甲斑蝥素(NCTD),通过抑制尿激酶型纤溶酶原激活物(uPA)而发挥抗黑色瘤转移的作用.方法 采用分子虚拟对接软件autodocking 4.0计算NCTD分子结构与uPA蛋白的空间结合能力,采用MTS的方法考察NCTD对uPA诱导B16F10细胞增殖的影响,并采用C57BL6小鼠的实验性转移模型考察NCTD在体内对黑色素瘤转移的影响,同时
INTRODUCTION Currently, hypoxia-induced epithelial mesenchymal transition is thought to be a key step for cancer metastasis.The development of metastasis requires the movement and invasion of cancer c
Object To research the inhibiting effects of acteoside extracted chemical composition from cistanche tubulosa on experimental begnin prostatic hyperplasia (BPH) in rats.Methods The begnin prostatic hy
The use of Dox is limited due to its association with cardiovascular complications, which are manifested as acute and chronic cardiotoxicity.The pathophysiological mechanism of it appears to involve a