Study On The Effect Of Endostar In Inhibiting The Growth Of Murine Liver Cancer H22

BACKGROUD:Malignant tumor has two characteristics which are unrestricted invasive growthand distant metastasis, angiogenesis is an important prerequisite for tumor infiltrate growth andmetastasis. Therefore, the inhibition of angiogenesis has far-reaching significance and broadprospects in tumor treatment. people’s.Because of poor targeting traditional anticancer drugsare easier to produce toxic side effects, antiangiogenic therapy provides a new approach fortumor treatment.In recent years, the role of anti-angiogenic agents inhibiting tumor formationand metastasis aroused great attention from scholars day by day.1997, ORilly et al found arelative molecular mass of20,000new protein, which is named for endostatin.China’s LiZhongyi, also found that the endostatin of human,and screening to clone the gene from humanliver cDNA library. First in china human soluble endostatin is expressed in yeast.This is theresearch of the anti-cancer Endostar mechanism was discussed.Objective: To observe the growth-inhibition of Endostar on murine liver cancer H22.Toinvestigate the mechanisms of Endostar in the treatment of cancer.Methods: The mice with H22were randomly divided into four groups:Model group、Low dose ofEndostar group、Middle dose of Endostar group、High dose of Endostar group. Intervention weregiven different drugs for7days, the changes in tumor volume of mice, tumor weight and tumorinhibitory rate were measured. Expression levels of Microvascular density in tumor tissue wereobserved by immunity histochemistry technology.Results: Beginning of the experiment, no difference in tumor volume in each group, the Fourthday after the experiment began, the intervention group were lower than the tumor volume growthrate of model group, the seventh day, the intervention group tumor volume was significantlysmaller than the model group (P <0.05), High dose of Endostar group tumor volume was lessthan the other group (P <0.05);The weight and of tumor in model group were higher than that inother three groups. The weight of tumor in High dose group (1.35±0.05)g, respectively, werelower than that in Low dose group (2.16±0.05)g. Microvascular density of the tumor inexperimental group were lower than those in model group, Low dose of Endostar group、Middledose of Endostar group、 High dose of Endostar group down-regulated expression ofMicrovascular density in tumor tissue(P<0.05).The effect of High dose therapy indown-regulating Microvascular density was stronger than that induced by Low dose group orMiddle dose group．Conclusion:1. Endostar significantly inhibited tumor cell growth on murine liver cancer H22, And in a dose-dependence.2. Endostar significantly inhibited tumor cell growth on murine livercancer H22, the induction of growth-inhibition may be associated with decreased expression ofMicrovascular density in tumor tissue.