| Objective: Breast cancer is a kind of hormone-dependent tumor. It'soccurrence and development is mainly related to the estrogen and estrogenreceptor(ER). The incidence of breast cancer will increase if mammary glandhas been exposed to the estrogen long term.7,12-demethylbenz[a]anthrancene(DMBA) is a polycylic aromatic hydrocarbons. It belongs toanthracene which contains four benzene rings, and has strong effect to causecancer. At present it has become a mature reagent to induce breast cancer in theanimal model of rats, because its strongly specificity and highly selectivity forthe mammary gland, but there is few reports about the comparison on the roleof DMBA between the female SD rats before and post menopause. Thisexperiment established the animal model of female SD rats with or withoutmenopause and observed effect of DMBA on them. HE dyeing was using toevaluate the status of tumors. The incidence of tumors, latency, the number andsize of tumors were compared among different groups. The influence of DMBAon different female SD rats with or without menopause was analyzed andwhether the role of DMBA on tumorigenesis depends on the estrogen wasfurther studied.Methods:166healthy female virgin SD rats of6weeks old were choosed and randomlydivided them into three groups:①experimental group contains22(giveDMBA by gastric lavage after spay one week),②the negative control groupcontains22(give DMBA),③the blank control group contains22(Normalfeed).2The experiment begining after all of the SD rats to adapt to raise one week.The experimental group and negative control group were given DMBA bygastric lavage twice, the single dose was10mg/100g, removed one week. The experimental group was given DMBA after spay one week, the blank controlgroup was given the same dose solvent.3The condition of the SD rats were observed every three to four days, themorbility, latency, the size and number of the tumors were recorded. During theexperiment, the rats were killed when the tumor was diabrosis and terminatedthe expriment. All of the rats were killed and anatomized after24weeks. Themorphological change were observed by macroscopy. Some of the normalbreast tissue and all of the tumor tissue were imbedded with paraffin andstained with HE.4The data was organized and processed with SPSS13.0statistical software, thesize of test was0.05.Results:1Incidence: When the experiment was ended, there were57rats survived in theexperiment, and27of them rats had breast tumors. There were17rats survivedin the experimental group, and9of them had tumors, the incidence was52.9%.There were18rats survived in the negative control group, and all of them hadtumors, the incidence was100%. There had no tumor in the blank control group.There was statistical difference among three groups (χ~2=40.021,P=0.000).There was statistical difference between every two groups of the three groups,the experimental group and negative control group, the experimental group andblank control group, the negative control group and blank control group(P=0.001; P=0.000; P=0.000).2Latency period: When the experiment was ended, the latency period in theexperiment group was136.67±39.83days, the negative control group was60.22±29.86days. There was statistical difference between the experimentgroup and negative control group(t=5.087, P=0.000).3Diameter of tumors: experiment group was1.56cm±0.98cm, negative controlgroup was12.67cm±7.33cm. There was statistical difference between the twogroups(t=-4.484, P=0.000).4tumor numbers: The17rats in the experimental group has9tumors,6of9were malignant tumors, the average tumor number of every mouse was0.53; The18rats in the negative control group has108tumors,91of108weremalignant tumors, the average tumor number of every mouse was6.0. Theexperimental group was obviously less than the negative control group, therewas statistical difference between the two groups (Z=-5.236,P=0.000).5Types of the tumors: When the experiment was ended, there were6rats hadmalignant tumors in the experiment group and there were3rats had atypicalhyperplasia, the incidence was35.3%and17.6%respectively. In the negativecontrol group, all of the rats had malignant tumors and only7rats had atypicalhyperplasia, the incidence was100%and38.9%respectively. There was notumors happened in the blank control group. After the statistical comparison,the incidence of malignant tumors among the three groups had statisticaldifference (χ~2=41.074, P=0.000). There was statistical difference betweenexperimental group and negative control group, experimental group and blankcontrol group, negative control group and blank control group (χ~2=16.985, P=0.000; P=0.004; χ~2=40.000, P=0.000). The incidence of atypical hyperplasiaamong the three groups had statistical difference (χ~2=10.350, P=0.006). Therewas no statistical difference between experimental group and negative controlgroup, experimental group and blank control group (P=0.264; P=0.074),however, the incidence of atypical hyperplasia between negative control groupand blank control group had statistical difference (P=0.002).Conclusion:1The animal model of breast cancer in rat can be made successfully by givenfemale SD rats10mg/100g DMBA intragastric administration twice. We canused the model to simulate the incidence and development of human breasttumor, and to study the mechanism in breast carcinogenesis and do variousintervention studies.2After castration, the latency period,tumor size of the breast cancer in thefemale SD rats had significantly difference compared with negative controlgroup, which show that ovariotomy can reduce the role of DMBA on inducingbreast cancer in female SD rat, to a large extent, DMBA depends on theexistence of estrogen to play its' carcinogenesis. 3Furthermore, in this experiment we can observe that the incidence rate ofatypical hyperplasia in negative control group is obviously higher than theblank control group, however, there have no statistical difference between theexperimental group and blank control group. The result shows that DMBAdepends on the existence of estrogen to play its' carcinogenesis. |
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