目的 探讨细胞骨架微管蛋白在牵张刺激心肌细胞肥大反应中的作用。方法 通过体外牵张培养的心肌细胞，采用3H-亮氨酸掺入法和四甲基偶氮唑盐微量酶反应比以法反映心肌细胞肥大指示和海参心肌细胞数目，激光共聚焦定性、定量微管蛋白的合成和分布情况。结果 20%的持续性牵张引起心肌细胞的3H-亮氨酸掺入量[12h为（1870.1±112.5）cpm，24h为（2015.5±19.37）epm]，与对照组[12h为（1122.7±12.5）epm，24h为（1210.7±222.7）cmp]比较显著增加，微管解聚剂秋水仙素（4μmol/L）可以明显抑制3H-亮氨酸掺入量[12h为（1292.7±142.6）epm，24h为（1327.8±97.4）epm]。牵张12h即可见微管蛋白荧光强度增强，24h部分细胞呈现微管蛋白结构坍塌，纹理模糊，荧光强度分布不均，微管蛋白最高光密度值1600（任意单位)，可被4μmol/L秋水仙素抑制。结论 细胞骨架微管蛋白系统是牵张刺激诱导心肌细胞肥大反应的细胞内信号传递途径之一。

A number of mechanical cell stimulators have been used to study the effect of mechanical stmulation on cells in vitro. But the efficiencey of these devices is not fully desirable. We recently developed a new device for mechaical cell stimulation, the centrifugal force stretcher, and compared its efficacy with that of the traditional Flexercell Strain Unit. When the mechanical stretcher circumrotates with certain speed, cardiac myocytes attached on the plate are stretched and elongated by centrifugal force. Neonatal rat cardiac myocytes were isolated by enzymatic dissociation from the hearts of 3～5d old Sprague Dawley rats, and were mechanically stimulated by traditional 20% strech and 180r/min centrifugal force for 12 and 24h. The effects of mechanical stimulation on the hypertrophic response of neonatal rat cardiac myocytes and production of angiotensin Ⅱ(Ang Ⅱ) were examined. Compared with the non-stretch group. the radioactivity of 3H-leucine incororated into the stretch-stimulated cardiac myocytes in the centrifugal force stretch group was significantly higher[(1295. 17±51.19)vs(1122.67±51.63) in 12h; (1447.5±35.96)vs(1210.67±90.92)in 24h, P<0.05].Ang Ⅱ was also dramatically increased by 128% in 12h (P<0.05) and 139% in 24h (P<0.01). After the myocytes was stretched for 24h, the LDH level in the mediun in the Flexercell Strain Unit group was significantly higher than that in the centrifugal force group [(14.5±8.7) U/L vs (7.8±4.3)U/L, and Ang Ⅱ secretion of the cardiac myocytes, and the damage to the cells bronght by this stimulator is relatively slighter in comparison with the Flexercell Strain Unit.

目的：探讨OxLDL在动脉粥样硬化血管局部免疫病理损伤中的作用机制。方法：采用地高辛标记的寡核苷酸控针原位杂交技术，观察OxLDL对人外周血单核细胞MCP-1、PDGF、bFGF、IL-104种致炎细胞因子mRNA表达的影响。结果：OxLDL（10～30mg/L）同人外周血单核细胞孵育24小时后能够以剂量依赖性方式显著提高MCP-1、bFGF、FDGF、IL-104种致炎细胞因子mRNA表达（均p<0.001）。结论：OxLDL能以剂量依赖性方式直接刺激人外周血单核细胞分泌致炎细胞因子mRNA。