论文部分内容阅读
目的:探讨雄性去势小鼠和正常小鼠Lewis肺癌移植瘤生长、性激素及其受体表达的差异,了解性激素对肺癌发生的作用机制。方法 :选用24只8~9周龄C57BL/6雄性小鼠,随机分为去势组和对照组各12只。去势组采用经腹部途径双侧睾丸切除术,对照组进行同一部位双侧睾丸周围脂肪切除的假手术。恢复性饲养2周后,采用腋下皮下接种法建立小鼠Lewis肺癌模型。观察各组小鼠体内肿瘤的生长情况,每5 d测量一次肿瘤大小。接种3周后,称取小鼠体质量并取血清,然后采用脱颈法处死小鼠,分别剖取移植瘤和肺组织并称质量。ELISA法检测去势组和对照组血清中雌二醇(estrodiol,E_2)和睾酮(testosterone,T)水平。免疫组织化学法检测小鼠移植瘤与肺组织中雄激素受体(androgen receptor,AR)和雌激素受体(estrogen receptor,ER)α/β的表达情况。结果 :与对照组比较,去势组小鼠术后体质量减轻(P<0.05),移植瘤体积增长较快(P<0.05),移植瘤和肺组织质量均明显增加(P值均<0.05),肺部转移结节数增多(P<0.05),血清中E_2和T水平均成倍降低(P值均<0.001)。去势组和对照组的肺组织中,AR、ERα和ERβ均高表达,且去势组的高表达率明显高于对照组(P值均<0.05);在移植瘤组织中,去势组和对照组的AR和ERα均低表达,而ERβ高表达,且去势组的ERβ高表达率明显高于对照组(P<0.05)。结论 :去势可引起小鼠体内性激素水平紊乱,性激素受体表达异常上调,从而使小鼠体质量减轻,移植瘤生长加速,肺部转移结节数增多。推测性激素及其受体水平失衡可能影响肺癌的发生和发展。
OBJECTIVE: To investigate the difference of growth, sex hormone and its receptor expression between Lewis ovarian cancer and transplanted Lewis lung carcinoma in castrated mice and normal mice to understand the mechanism of sex hormones on lung carcinogenesis. Methods: Twenty-four C57BL / 6 male mice aged 8-9 weeks were randomly divided into two groups: castrated group and control group. Castration group by bilateral abdominal orchidectomy, the control group of the same site bilateral fat testis around the false surgery. Two weeks after the recovery, mice model of Lewis lung carcinoma was established by subcutaneous axillary subcutaneous inoculation. The growth of tumor in each group was observed and the tumor size was measured every 5 days. Three weeks after inoculation, the mice were weighed, serum taken, and mice sacrificed by cervical dislocation. The xenografts and lung tissues were taken and weighed. The levels of estrodiol (E_2) and testosterone (T) in serum of castration group and control group were detected by ELISA. Immunohistochemistry was used to detect the expression of androgen receptor (AR) and estrogen receptor (α / β) in the xenografts and lung tissues of mice. Results: Compared with the control group, the body weight of the mice in the ovariectomized group was significantly decreased (P <0.05), the volume of the transplanted tumor increased rapidly (P <0.05), and the quality of the xenografts and lung tissues were significantly increased ), Pulmonary metastasis nodules increased (P <0.05), serum E2 and T levels were doubled (P <0.001). In the castrated and control groups, AR, ERαand ERβwere highly expressed, and the high expression rate in the castration group was significantly higher than that in the control group (all P <0.05). In the xenograft tumors, The expression of ERβ and ERβ in ovariectomized group were significantly lower than those in control group (P <0.05). CONCLUSION: Castration can cause sex hormone levels disorder in mice and abnormally up-regulated expression of sex hormone receptors, thereby reducing the body weight of mice, accelerating the growth of xenograft tumors and increasing the number of pulmonary metastatic nodules. Speculated that the imbalance of sex hormones and their receptors may affect the occurrence and development of lung cancer.