中文摘要：

目的通过体外实验研究导痰汤是否能通过调节c—Jun氨基末端激酶（JNK）信号通路来干预细胞间黏附分子-1（ICAM—1）的表达，以揭示导痰汤治疗动脉粥样硬化的机制。方法培养人脐静脉内皮细胞（HuVEc），并随机分为7组。空白对照组：正常培养HUVEC24h；导痰汤对照组：用20％导痰汤含药血清预处理HUVEC6h；肿瘤坏死因子-a（TNF-a）诱导组：用200kU／L TNF—a培养HuVEC12h；5％、10％、20％导痰汤干预组及JNK阻滞组：TNF—a诱导前分别给予5％、10％、20％导痰汤含药血清或25umol／L JNK特异性阻滞剂SP600125预处理。采用聚合酶链反应（PCR）和蛋白质免疫印迹法（western blotting）检测HUVEC中ICAM-1mRNA和JNK蛋白的表达。结果TNF—a诱导组ICAM-1 mRNA和JNK蛋白表达显著高于空白对照组和导痰汤对照组（均P〈0．01）；用导痰汤含药血清或SP600125预处理，ICAM-1mRNA和JNK蛋白表达显著下降（P〈0．05或P〈0．01）。JNK蛋白与ICAM-1mRNA水平呈显著正相关（r=0．680，P〈0．01）。结论导痰汤可以有效抑制TNF—a刺激所致的HUVEC中ICAM-1的过度表达，这可能与导痰汤可抑制JNK信号通路有关。

英文摘要：

Objective To study whether Daotan decoction （导痰汤, DTD） may through the regulation on c-Jun N-terminal kinase （JNK） pathway interfere the expression of intercellular adhesion molecular-1 （ICAM-1） in human umbilical vein endothelial cells （HUVECs） and to explore the mechanism of DTD for treatment of atherosclerosis by an experiment in vitro. Methods HUVEC were cultured in vitro and divided into seven groups： blank control group, DTD serum control group, tumor necrosis factor-a （TNF-a） group, 5%DTD serum group, 10% DTD serum group, 20% DTD serum group, JNK inhibitory group. The cells were cultured for 24 hours in the blank control group. The cells were pretreated with serum containing 20% DTD for 6 hours in the DTD serum control group. In TNF-a inducing group, 200 kU/L TNF-a was added in the HUVEC culture for 12 hours. In 5%, 10% and 20%DTD interference groups and JNK inhibitory group, before the induction of TNF-a, the HUVEC culture was pretreated respectively with DTD serum （5%, 10%, 20%, 6 hours） or SP600125 （a JNK blocking agent, 25 umol/L, 30 minutes） and then co-treated with 200 kU/L TNF-a for 12 hours. The ICAM-1 mRNA and JNK protein expressions in HUVEC were observed by polymerase chain reaction （PCR） and Western blotting methods. Results Compared with two control groups, the expressions of ICAM-1 mRNA and JNK protein in TNF-a group were significantly increased （all P〈0.01）. And compared with TNF-a group, the serum containing DTD or after SP600125 treatment could significantly restrain ICAM-1 mRNA and JNK protein expressions （P〈0.05 or P〈0.01）. Also, there was significant positive relationship between the level of ICAM-1 mRNA and JNK protein （r= 0. 680, P〈 0. 01）. Conclusion DTD can effectively restrain ICAM-1 expression which is induced by the stimulation of TNF-a in HUVEC, that is possibly related to the inhibitory action of DTD on JNK pathway.