目的 研究艾葉制炭前后對(duì)人主動(dòng)脈內(nèi)皮細(xì)胞組織因子途徑抑制物（TFPI）、內(nèi)皮細(xì)胞血管性假血友病因子（vWF）、NO含量的影響，以及對(duì)大鼠血小板氨基末端激酶-1（JNK1）表達(dá)水平的影響，闡明艾葉炭止血機(jī)制。方法 將體外培養(yǎng)的人主動(dòng)脈內(nèi)皮細(xì)胞（HEAC）隨機(jī)分組，分別給予不同極性（石油醚、二氯甲烷、醋酸乙酯、正丁醇、水、水提物、鞣質(zhì)、總黃酮）部位的艾葉生、炭品，終質(zhì)量濃度為200、100、50 μg/mL，培養(yǎng)48 h后，取細(xì)胞培養(yǎng)液試劑盒法測(cè)定TFPI、vWF、NO含量；采用免疫蛋白印跡方法檢測(cè)艾葉制炭前后各部位對(duì)大鼠血小板JNK1磷酸化水平的影響。結(jié)果 與對(duì)照組及相應(yīng)生品組比較，艾葉炭品二氯甲烷和鞣質(zhì)部位TFPI、NO含量顯著降低，vWF含量顯著升高（P<0.01）；大鼠血小板JNK1磷酸化水平顯著升高（P<0.01）。與對(duì)照組比較，艾葉鞣質(zhì)部位TFPI、NO含量顯著降低，vWF含量顯著升高（P<0.01）；大鼠血小板JNK1磷酸化水平顯著升高（P<0.01）。結(jié)論 二氯甲烷和鞣質(zhì)部位是艾葉炭的主要止血作用部位，其止血機(jī)制為降低TFPI、NO含量、增加vWF的含量；明顯提高血小板JNK1的磷酸化水平。

Objective To investigate the effect of Artemisiae argyi Folium being charred on the content of TFPI, vWF, NO in HAEC, and JNK1, and to clarify the haemostatic mechanism of Artemisia argyicarbonisatus and part of the mechanism of platelet activation. Method The HEAC cultured in vitro were randomly divided into groups, which were given different polar parts of Artemisiae argyi Folium and Artemisia argyicarbonisatus with final concentration of 200, 100, and 50 μg/mL. The content of of TFPI, vWF, NO in cell culture fluid were measured by Kit after HEAC were cultured 12 h, measured the effect of Artemisiae argyi Folium before and after being charred on rat platelet JNK1 phosphorytion level. Results Compared with control group and the corresponding raw products group, the content of TFPI and NO in dichloromethane and tannin of Artemisia argyicarbonisatus decreased significantly, the content of vWF increased significantly (P<0.01), and the level of platelet JNK1 phosphorylation in rats increased significantly (P<0.01). Compared with the control group, the content of TFPI and NO in tannin of Artemisiae argyi Folium decreased significantly, and the content of vWF increased significantly (P<0.01), and the level of platelet JNK1 phosphorylation in rats increased significantly (P<0.01). Conclusion Dichloromethane and tannin sites are the main hemostasis part of Artemisia argyicarbonisatus, its hemostatic mechanism is to reduce the content of TFPI and NO, increase the content of vWF, and increase the level of phosphorylation of platelet JNK1 obviously.

艾葉炭炮制原理研究國家自然基金資助項(xiàng)目（81173545）