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作 者:张大雷[1] 周玲 邹挺[1] 杨蓓[1] 吴磊[1]
机构地区:[1]南昌大学医学院,南昌330006 [2]南昌市卫生学校,南昌330006
出 处:《中国细胞生物学学报》2010年第3期404-408,共5页Chinese Journal of Cell Biology
基 金:国家自然基金资助项目(No.30960409);江西省教育厅资助项目(No.GJJ09112)~~
摘 要:利用精原细胞-体细胞体外无血清共培养模型研究了卵泡刺激素(FSH)和17-β雌二醇(E_2)对小鼠A型精原细胞增殖的影响。结果表明:FSH(10 ng/m1)可显著增加精原细胞集落数目,蛋白激酶A(PKA)抑制剂H_(89)可抑制FSH对精原细胞的促增殖作用,说明FSH(10 ng/ml)可通过PKA介导的信号途径促进A型精原细胞增殖。E_2能够促进小鼠A型精原细胞的增殖,而雌激素受体阻断剂他莫西芬(tamoxifen)可抑制E_2的促增殖作用,说明E_2是直接通过雌激素作用与睾丸细胞上受体结合进而调控精原细胞的发育。此外,FSH(10 ng/ml)联合E_2(10^(-8)~10^(-7)mol/L)具有加性效应。The serum-free spermatogonium-somatic cell coculture model was used to evaluate the effects of follicle-stimulating hormone (FSH) and epidermal 17β-estradiol (E2) on proliferation of mouse type A spermatogonial cells. Results showed that FSH (10 ng/ml) significantly increased spermatogonial colony number and the proliferating effect was blocked by PKA inhibitor H89. These results suggested that FSH stimulated the proliferation of mouse spermatogonia involving activation of PKA signaling pathway. E2 (10^-7-10^-6 mol/L) promoted proliferation of type A spermatogonia and the promoting effect of E2 was inhibited estrogen receptor antagonist tamoxifen (0.1 mg/mL). These results indicated that E2 exerted direct estrogenic action to regulate spermatagonial development via estrogen receptors expressed in the testis. Furthermore, FSH (10 ng/ml) could synergize with E2 (10^-8-10^-7 mol/L) to promote spermatagonial proliferation.
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