消痰利水酊剂对艾氏腹水瘤小鼠作用的实验研究

目的]研究消痰利水酊剂对艾氏腹水瘤（EAC）小鼠的作用及其可能的机制。方法]昆明种实验小鼠腹腔内注射0．2mlEACE2G8细胞株悬液（瘤细胞浓度4×10^6／ml）制备腹水瘤小鼠模型。成模小鼠分为荷瘤（对照）组、消痰利水酊剂（酊剂）组、环磷酰胺（CTX）组、酊剂加CTX（联用）组，分别给予荷瘤对照、腹壁外用消痰利水酊剂、腹腔注射CTX、腹壁外用酊剂加腹腔注射CTX联用。观察各组小鼠体重、死亡后排净腹水之净体重、死亡时腹水重量、生存时间，ELISA法检测各组腹水上清液血管内皮生长因子（VEGF）、肝素酶（HPA）水平。结果]酊剂组可降低荷瘤小鼠种瘤后o～12d体重恶化趋势（P〈0．05），与CTX腹腔注射联用可加强此作用（P〈0．05），并能减少小鼠死亡时腹水量（P〈0．05），有效提高荷瘤小鼠死亡时净体重（P〈0．05），效果优于单纯予以CTX（P〈0．05）。酊剂组、CTX组、联用组均能明显降低小鼠腹水上清液中HPA水平（P〈0．05）。但各组生存时间差异无统计学意义（P〉0．05）。结论]消痰利水酊剂与CTX联用更可加强延缓艾氏腹水瘤小鼠体重变化，抑制恶性腹水的生成，增加小鼠净体重，改善小鼠生存质量，减少化疗部分不良反应。其作用机制可能与下调腹水中HPA的水平从而降低腹膜及血管通透性相关。

Survival effect and mechanisms of Xiaotan Lishui Tincture on mice bearing Ehrlich ascites carcinoma cell

Objective]To investigate the survival effects of Xiaotan Lishui Tincture（XLT） on mice bearing Ehrlich ascites carcinoma（EAC） cell and its possible mechanism. Methods]Mouse EAC model was established by intraperitoneal injection of 0. 2 ml E2G8 ascitic cells（concentration 4×10^6/ml） and the animals were subsequently divided into 4 groups randomly： tumor control group,XLT group（external abdominal skin with XLT）, CTX group（intraperitoneal injection of CTX） , XLT＋CTX group（topical XLT combined with intraperitoneal injection of CTX）. The body weight changes, mouse net weight at the death, ascites weight at the death, survival time, and Elisa evaluation of vascular endothelial growth factor（VEGF） and heparinase（HPA） expressions in ascites were observed. Results] XLT group reduced the deteriorating trend of body weight of tumor-bearing mice in the 0-12 days（P〈0. 05）, the role of XLT＋CTX group was more significantly （P〈0. 05）. And XLT＋CTX group could reduce malignant ascites formation（P 〈0. 05） ,improved the net weight at the death of mice（P〈0. 05）, better than simply with CTX （P〈0. 05）. XLT group, CTX group, XLT＋CTX group significantly reduced HPA concentration in ascites（P〈0.05）. There was no significant difference in all groups of mice of survival time, VEGF concentration in ascites（P〉0. 05）. Conclusion]The treatment of XLT reduces the deteriorating trend of body weight, combined with intraperitoneal injection of CTX resultes in a strengthening role of this trend and a decrease in the ascites weight with a concomitant increase in life quality of the EAC cell-bearing mice, but can not extend the survival time. These results probably can be explained by reducing the HPA level in ascites to cut down the peritoneal and vascular permeability.