胎肾细胞悬液对去势大鼠骨组织不同部位ER-α表达的影响

摘要

目的 探讨胎肾细胞悬液(fetal renal cell suspension,FRCS)对去势大鼠骨组织雌激素受体(ER-α)表达的影响,为“肾主骨”理论提供实验依据.方法 4月龄SD雌性大鼠随机分成假手术组、模型对照组、雌激素组、胎肾细胞悬液组,假手术组仅去除卵巢周围脂肪,给药组在去除卵巢后4周分别给予雌二醇及FRCS,4周后处死所有大鼠,HE染色观察骨组织形态学变化,放免法测定血清E2水平,免疫组化检测ER-α在股骨干骺端不同部位的阳性表达情况.结果 与假手术组相比,模型对照组骨小梁稀疏,排列紊乱,骨小梁间隙增大明显,血清E2水平明显下降(P＜0.01);与模型对照组比较,雌激素、胎肾细胞悬液两组骨小梁连续,排列整齐,E2水平升高(P＜0.01).子宫指数的变化与血清E2类似.与假手术组比较,模型对照组ER-α在股骨干骺端关节软骨、骺板软骨、骺板下初级小梁骨、髓腔的表达均明显下降(P均＜0.05),与模型对照组比较,雌激素与胎肾细胞悬液组各部位ER-α表达明显升高(P均＜0.05).结论 FRCS可通过调控骨组织中ER-α的表达发挥抗骨质疏松作用.%Objective To investigate the effect of FRCS on expression of bone ER-oin rats with ovariectomy so as to provide evidence for the theory that the kidney dominates bones.Methods Four-month-old Sprague Dawley female rats were randomly divided into sham operated group,model control group,estrogen treatment group and FRCS treatment group.Only the fat around the ovary was removed in sham operated group,while ovaries were removed in other groups.Four weeks after operation,estrogen and FRCS were administered to rats of treatment groups respectively,and the treatment lasted four weeks.Then,the bone morphology was evaluated by HE stain,the serum level of E2 was detected by radio-immunity,the protein expression of ER-α in cells of the bone tissue surface was investigated by immunohistochemical method.Results Compared with sham operated group,the bone trabecula in model control group was sparce and disorderly,the trabecular interspace was enlarged more obviously,and the serum level of E2 decreased (P ＜ 0.01).Compared with model control group,the serum level of E2 in estrogen treatment group and FRCS treatment group increased(P ＜0.01)and the bone brabecula was more continual and aligned in boner order,the uterus index changed as serum E2 did.Compared with sham operated group,the expression of ER-α decreased in the articular cartilage,epiphyseal plate,bone trabecula and bone marrow(All P ＜ 0.05) in model control group.Compared with model control group,the expression of ER-α increased in estrogen treatment group and FRCS treatment group(All P ＜ 0.05).Conclusions The mechanism by which FRCS can prevent and cure postmenopausal osteoporosis may lie in the ability of FRCS to modulate the expression of bone ER-α.