摘要
目的探讨血管内皮抑制素腹腔内给药对H22小鼠腹水瘤生长及腹水的抑制作用。方法取110只昆明小鼠腹腔内接种H22细胞(2×106细胞/只),建立小鼠腹水瘤模型,接种后随机分为5组:模型对照组(0.9%NS);低剂量血管内皮抑制素组(4mg/kg);中剂量血管内皮抑制素组(8mg/kg);高剂量血管内皮抑制素组(12mg/kg);阳性对照组(顺铂0.6mg/kg)。接种24h后连续10d给予各药物腹腔内注射,停药24h后处死各组小鼠,测量腹水量并取腹水行相关检测;解剖小鼠,观察腹腔脏器及肺脏的转移情况;通过Evan蓝的吸光度值反映小鼠的腹膜渗透性;观察各组小鼠的生存时间。结果与模型对照组相比,中、高剂量血管内皮抑制素组可显著抑制荷H22腹水瘤小鼠腹水的生成,并减少腹腔内及肺脏转移,延长生存时间。结论血管内皮抑制素腹腔内用药治疗荷H22腹水瘤小鼠腹水具有显著的抑制作用。
Objective To investigate the effect of intraperitoneal endostar administration to treat H22 ascites in mice. Methods A mouse model of ascites was established by inoculating 110 Kunming mice with H22 cells （2×10^6,i.p. injection）.Mice were then divided randomly into 5 groups：control （normal saline） ;low endostar dose （ 4 mg/kg. day ）, intermediate endostar dose （8 mg/kg. day ）, high endostar dose（ 12 mg/kg.day）and positive control（DDP 0.6 mg/kg.day）.After an adjustment period of 24h,the groups were treated from day 1 to day 10 by i.p. injection as indicated above and sacrificed 24h after drug withdrawal.Data were collected on volume of ascitic fluid, metastases of abdominal organs and lungs and survival time.Peritoneal membrane permeability was assessed using Evan blue staining. Results Intermediate and high doses of endostar significantly inhibited the production of ascites in H22 ascitesbearing mice,reduced the frequency of metastases in the abdominal viscera and lungs,and lengthened average survival time. Conclusion Intraperitoneal administration of endostar can reduce ascites in H22 ascites-bearing mice.
出处
《中国癌症防治杂志》
CAS
2012年第2期153-157,共5页
CHINESE JOURNAL OF ONCOLOGY PREVENTION AND TREATMENT
基金
广西壮族自治区卫生厅科研课题(Z2009251
Z2009240)
