中文摘要：

【目的】研究丹参素钠（salvianicacidAsodium，SAAS）对小鼠黑色素瘤细胞株B16细胞间缝隙连接（GJIC）的影响及其机制。【方法】采用四甲基偶氮唑盐（MTF）法检测SAAS对B16细胞生长的影响，荧光显微镜观察及流式细胞仪荧光示踪法结合分析缝隙连接（GJ）功能变化，并与阳性对照药全反式维甲酸（ATRA）比较，采用westernblot法分析缝隙连接蛋白Cx32和Cx43的表达。【结果】以0-8μmol／L SAAS处理B16细胞48h不影响其生存；用0、1、2、4、8μmol／LSAAS处理细胞48h后，荧光显微镜下观察,sAAs能明显提高B16细胞Calcein传递，流式细胞术分析对照组和试验组的绿色荧光细胞（G4）与双阴性受体细胞（G3）比值（G4／G3）分别是0．10±0．01、0．16±0．02、O．20±0．01、0．21±0．02和0．25±0．02，各试验组G4／G3值显著高于对照组（P〈0．01）；Westernblot分析结果显示：用0、1、2、4、8μmoi／LSAAs处理细胞48h能显著提高Cx32、Cx43的表达。【结论】体外较低浓度SAAS能够促进B16细胞细胞间缝隙连接功能，但在一定药物浓度作用后．不能再提高其功能。SAAS促进GJ机制可能是通过上调Cx32、Cx43蛋白表达途径。

英文摘要：

Objective To study effects of salvianic acid A sodium （SAAS） on the gap junction function in mice melanoma cell line B16. Methods Inhibitive effect of SAAS on the growth of B16 cells was examined by MTT method, the gap junction function was analyzed by fluorescent tracer and flow cytometer under fluorescence microscope. The expression of connexins Cx32 and Cx43 was detected by Western blotting. All-trans-retinoic acid （ATRA） served as the positive control drug. Results Treatment with 0-8 μmol/L SAAS for 48h had no effect on the survival of B16 cells. Treatment with 0, 1, 2, 4, 8 μmol/L SAAS for 48h showed obvious effect on B16 cells. Calcein diffusion between B16 cells was enhanced under fluorescence microscope, flow cytometer analysis showed the ratio of Caleein labeled cells （G4） to double negative receptor cells （G3） was 0.10± 0.01, 0.16± 0.02, 0.20 ± 0.01, 0.21 ±0.02 and 0.25 ± 0.02 respectively, and the G4/G3 of experimental groups was significantly higher than that in the control group （P〈0.01） . Western blotting results showed enhancement effect on the expression of Cx43 and Cx32 protein in B16 cells by 0, 1, 2, 4, 8 μmoL/L SAAS. Conclusion Low-concentration SAAS could competently promote the gap junction function of B16 cells in a dose-dependent way in vitro within certain concentration, and its biological effect may be achieved through the up-regulation of the Cx43 and Cx32 expression.