摘要
目的旨在探讨补肾调肝法对自身免疫性卵巢早衰小鼠卵巢促卵泡生成素受体(FSHR)mRNA表达的影响。方法随机将60只小鼠分为6组,5组制作免疫性小鼠卵巢早衰模型(分别为模型组、西药组、中药高剂量组、中药中剂量组和中药低剂量组),另设1组为空白对照组。造模成功后第6天开始各药物组灌胃给药。连续灌胃4周后摘眼球取血,取卵巢组织待测。采用RT-PCR方法研究免疫性卵巢早衰小鼠的卵巢FSHR mRNA表达。结果卵巢FSHR mRNA表达模型组高于空白对照组,用药后表达均降低,总体趋势:中药高剂量组>西药组>中药中剂量组>中药低剂量组。结论补肾调肝方剂对自身免疫性卵巢早衰小鼠有一定的治疗作用,其治疗机理主要通过纠正紊乱的生殖内分泌轴,调动下丘脑—垂体—卵巢的生殖功能,改善临床症状,进一步对免疫性卵巢早衰起到一定的防治作用。
Objective To explore the influence of invigorating kidney and regulating liver method on the FSHR mRNA expression in ovary of autoimmune premature ovary failure mice. Methods 60 mice were randomly divided into 6 groups, 5 groups ( model group, western medicine group,high-dose TCM group,middle-dose TCM group and low-dose TCM group) were established the animal models of autoimmune premature ovary failure, the other group as blank control group. After the models have been established successfully, the mice were feed medicine on the 6th day separately. After feeding continuously for 4 weeks, eyeballs were taken off for taking blood, then execute the mouse and took the ovary tissue for testing, RT-PCR were used to exam the mRNA expression of the FSHR of the ovary. Results The FSHR mRNA expression of ovary in model group was higher than blank control group, after drug administration, the descending trend of FSHR mRNA expression of ovary was high-dose TCM group 〉 western medicine group 〉 middle-dose TCM group 〉 low-dose TCM group. Conclusion The Chinese herbal medicine of invigorating the kidney and regulating the liver could possibly treat the autoimmune premature ovary failure. The basis of the treatment was regulating and inspiring the disorder of reproductive endocrine axis, activating the function of hypothal- amus-pituitary-ovary,improving the clinical symptom, thus prevent the autoimmune premature ovary failure.
出处
《疑难病杂志》
CAS
2010年第3期174-176,共3页
Chinese Journal of Difficult and Complicated Cases
基金
教育部高等学校博士学科点专项科研基金(新教师基金)(No.20070026036)
关键词
补肾调肝法
卵巢早衰
自身免疫性
促卵泡生成素受体
小鼠
The method of invigorating kidney and regulating liver
Premature ovary failure, autoimmune
FSH receptor
Mice