机构地区:[1]南昌大学第二附属医院肝胆外科,江西南昌330006
出 处:《中国临床医学》2006年第5期750-752,共3页Chinese Journal of Clinical Medicine
基 金:国家自然基金资助课题(基金编号39960084)
摘 要:目的:探讨胆汁胆固醇对胆囊平滑肌线粒体及TGF-β1表达的影响及作用机制。方法:64只实验豚鼠随机分为4组,每组16只:对照组(标准颗粒饲料饲养2周),高胆固醇组(标准颗粒饲料加入2%高胆固醇饲养2周)、自然恢复组(高肛固醇组2用后,标准颗粒饲料饲养2周)和治疗组(高胆固醇组2周后,标准颗粒饲料+中药灌胃2周)。各组豚鼠实验到期后,腹腔麻醉后剖腹测量胆囊体积,记录胆汁量,测量胆汁中胆固醇浓度。取胆囊全层约1 mm3的组织,按常规制作电镜标本,采用图像分析仪观察胆囊平滑肌细胞线粒体平均体积(V)及数密度(Nv)。利用蛋白免疫印迹分析的方法测定其余胆囊组织活化TGF-β1的含量。结果:经高胆固醇饲养2用后,高胆固醇组豚鼠胆囊平滑肌细胞线粒体的平均体积(V),数密度(Nv)与对照组相比分别显著性升高(0.081)56±0.0069 vs 0.0653±0.02868,P<0.001)和下降(0.2677±0.0138 vs 0.3180±0.02868,P<0.001)。高胆固醇组豚鼠胆囊平滑肌组织活化TGF-β1与对照组相比显著升高(P< 0.001)。治疗2用后与自然恢复组比较,治疗组线粒体平均体积(V)下降(0.0715±0.0113 vs 0.0778±0.0092,P<0.001),而数密度上升(0.3086±0.0230 vs 0.2681±0.0128,P<0.001),胆囊平滑肌组织活化的TGF-β1明显下降(P=0.000)。结论:清热利胆理气活血方药可改善线粒体功能,下调活化TGF-β1的表达促进胆囊收缩功能的恢复,其作用机制可能与降低胆汁中胆固醇有关。Objective:To investigate the effect of cholesterol on the mitochondria and TGF-β1, of gallbladder smooth muscle. Methods:Sixty-four guinea pigs were randomly divided into four groups, every group contains 16 guinea pigs. The control group was fed standard chow, while the high-cholesterol group was fed standard chow plus 2% cholesterol, after two weeks', the natural group was fed standard chow and the treated group was received oral administration of the traditional Chinese medicine. Gallbladder were exposed with a midline incision under anesthesia and gallbladder volume was measured and the bile was aspirated to measure its volume and concentration of bile cholesterol. Gallbladder was removed from the liver bed intactly. A small mass of gallbladder(about 1 cm3 ) was obtained for electron-microscope, then the morphosis was observed and the mean volume(V) and the numerical density(Nv) of mitochondrial of smooth muscle cells were counted by an image analysis system. The rest gallbladder tissues were used to study the expression of active form TGF-β1 using Western Blotting. Results: (1) Compared with control group, after the two-week high-cholesterol feeding, the mean volume(V) of mitochondria was increased (0. 08056±0. 0069 vs 0. 0653±0. 02868, P〈0. 001 ) and the numerical density(Nv) of it was decreaed(0. 2677±0. 0138 vs 0. 3180±0. 02868,P〈0. 001). (2)Compared with control group, after the two-week high-cholesterol feeding, the expression of active form TGF-β1 increased(P〈0. 001). (3)After two-week treatment, compared the natural group, the concentration of bile cholesterol, the mean volume(V) and the numerical density(Nv) of mitochondria and the expression of active form TGF-β1 come back to normal. Conclusion:CSRA principle can restore the gallbladder contractile function by recovering the morphological changes of mitochondria and down-regulating the expression of active form TGF-β1. The mechanism is correlated with reducing bile choleste
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