实验性更年期抑郁症动物模型的建立和评价

Establishment and evaluation of experimental animal models of involutional depression

目的:建立一种有效、可行的更年期抑郁症动物模型。方法:采用雌性SD大鼠卵巢切除与慢性长期不可预见刺激相结合,建立更年期抑郁症的动物模型。共分正常组、抑郁症组、更年期组和更年期抑郁症模型组,每组10只。采用Open-Field行为学评分,糖水消耗实验,采用免疫荧光化学法测定血清雌二醇、黄体生成素、尿促卵泡素;免疫组化法测定下丘脑5-羟色胺、促性腺激素释放激素。结果:更年期抑郁症模型组水平活动积分为22.80±6.65,垂直活动积分为7.20±3.26,糖水消耗量为(73.3±19.0)mL,与正常组比较,差异均有显著性意义(t=7.12～9.54,P<0.01)。更年期抑郁症模型组雌二醇、尿促卵泡素和黄体生成素分别为(114.25±29.45),(0.47±0.11)和(0.19±0.05)μg/L,与正常组比较,差异均有显著性意义(t=5.34～8.23,P<0.01)。更年期抑郁症模型组5-羟色胺和促性腺激素释放激素含量分别为(48.4±21.3)和(170.2±44.6)个/视野,与正常组比较,差异均有显著性意义(t=3.25～9.87,P<0.01)。结论:该动物模型生殖内分泌激素与神经递质两方面均较好地反映了更年期抑郁症的病理生理变化。

AIM:To establish an effective and feasible involutional depression animal model. METHODS:Animal model of involutional depression were established by resecting the ovary of female SD rats combined with chronic unpredictable stimulation,and then they were divided into normal group,depression group,menopause group and involutional depression group with 10 rats in each group.Open Field locomotor scores and sugar water consumption test were used. Serum estradiol(E2),luteinizing hormone(LH) and follide stimulating hormone(FSH) were determined by using immunofluorescent chemistry,while the 5 hydroxythyptamine(5 HT) and gonadotrophin releasing hormone(GnRH) were measured with immunohistochemistry. RESULTS:The integrations of horizontal activity(22.80±6.65) and vertical activity(7.20±3.26),and the consumption of sugar water[(73.3±19.0) mL] in the menopause depression group were significantly different from those in the normal control group(t=7.12 to 9.54,P< 0.01).The E2,FSH and LH in the menopause depression group were(114.25±29.45),(0.47±0.11) and(0.19±0.05) μg/L respectively,significantly different from those in the normal control group(t=5.34 to 8.23,P< 0.01).There were significant differences in the contents of 5 HT and GnRH between the menopause depression group[(48.4±21.3) and(170.2±44.6) per visual field] and the normal group(t=3.25 to 9.87,P< 0.01). CONCLUSION:This animal model reflects the physiopathological changes of menopause depression disease in the aspects of productive endocrine hormone and neurotransmitter.