摘要
目的:探讨化癥口服液对荷H22小鼠的抗肿瘤作用和可能的机制。方法:75只健康小鼠随机分为5组,即空白对照组、荷瘤模型组、化癥口服液高、中剂量组(简称高、中剂量组)和阳性对照组。除空白对照组外,其余4组小鼠均以皮下注射瘤细胞悬液,0·2ml/只造模。于造模第2天,空白对照组和荷瘤模型组小鼠以生理盐水(NS)灌胃。高、中剂量组小鼠分别予100%、50%浓度的化癥口服液10ml/kg灌胃,2次/d,共10天。阳性对照组小鼠以CTX10ml/kg腹腔内注射,隔日1次,共5次。免疫组化方法检测瘤体内突变的p53蛋白;放射免疫法测定小鼠血浆内皮素(ET)水平。结果:荷瘤模型组小鼠的突变型p53表达水平明显高于其他3组(P<0·05),3个治疗组小鼠突变型p53表达都有不同程度的下降,3组间比较差异无显著性意义(P>0·05);模型组小鼠血浆ET水平明显高于空白对照组(P<0·001),其余各组的比较,ET水平均有不同程度下降,尤以高剂量组接近空白对照组水平,且与中剂量组和阳性对照组相比,差异有显著性意义(P<0·05)。结论:化癥口服液可以降低突变型p53蛋白表达,降低血浆ET水平并减少肿瘤的血供,这可能是其发挥抗肿瘤作用的机制之一。
Objective: To investigate the antitumor effect of HuaZheng Koufuye on mice bearing H22 and its possible mechanism. Methods: Seventy-five healthy mice were divided into 5 groups randomly: the normal group, the cancerbearing model group, the high dose group, the middle dose group and the positive group. Except the nomal group, the other 4 group were hypodermic injectel with oncocyte suspension 0. 2ml per mouse. From the second day, the mice of the control group and the model group were given sodium chloride by gastrolavage. The mice of the high dose and low dose group were given by gastrolavage with 100% and 50% Huazheng Koufuye 10ml/kg, twice daily for ten day, respectively. The mice of the postive group were intraperitoneal injected with 10ml/kg CTX once in two days'time. The immunohistochemistry assay was used to detect the expression of p53 in tumor tissue, the radioimmunoassay was used to detect the level of ET in plasma of each group. Results: The level of p53 protein expression in the model group was much higher than the other 3 groups ( P 〈 0. 05), but there were no significant differences among the 3 groups. The ET content in the model group was the highest, while in the normal group was the lowerest, though the ET level reduced in the other 3 groups, the high dose group decrease obviousely and near to the normal group, there was great difference between high dose group and the other 2 groups still. (P 〈 0, 05 ) , Conclusion: Huazheng Koufuye can inhibit the tumor growth and reduce its vascular service perhapse by down-regulating the expression of mutant p53 and plasma ET content, This may be one its antitumor mechanisms.
出处
《中西医结合肝病杂志》
CAS
2006年第5期275-277,共3页
Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
基金
湖北省自然科学基金项目(No.2004ABA237)