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近期研究提示,黄体萎缩(溶解)与细胞凋亡有关.但是影响细胞凋亡的因素还不清楚.我们以往的工作表明,抑制素α亚单位-N末端片段[Tyr]-1-32(P~(33))显著抑制大鼠黄体细胞孕酮分泌.本研究应用PMSG-hCG诱导大鼠的假孕模型进一步观察P~(33)以及其他因素对黄体细胞凋亡的作用.未成年大鼠注射65IU PMSG,48h后注射hCG50IU.于hCG注射第5天用P~(33)(40μg/只),P~(29)(37～65氨基酸)(50μg/只),催产素(oxytocin.OT)(40μg/只).Tyr(1.5mg/只)和E_2(1.5mg/只)每日一次:PGF_(2α)(12.5μPg/只)隔日注射.共注3次.于hCG注射第12天断头取血、卵巢.P~(33),P~(29).OT,PG_(2α)和Tyr处理组大鼠血浆雌激素、孕酮水平下降.E_2处理组则血浆雌激素、孕酮水平上升.提取DNA、定量、电泳分析显示.细胞核孵育后则可见清晰梯形条带.P~(33).P~(29).OT、PGF_(2α)和Tyr组直接提取或细胞核孵育后提取的低分子量DNA均增加.相反雌激素抑制低分子量DNA的产生.结果揭示、P~(29),P~(33)、OT.PGF_(2α).Tyr和雌激素在调节共黄体萎缩中起重要作用.P~(29),P~(33),OT.PGF_(2α).Tyr诱导大鼠黄体细胞介导凋亡的核酸内切酶的表达,促进黄体细胞凋亡;雌激素抑制黄体细胞凋亡.本结果对进一步探讨黄体细胞凋亡机制奠定了基础.
Recent studies suggest that luteal atrophy (lysis) is related to apoptosis, but the factors that affect apoptosis are not clear.Our previous work showed that the inhibin alpha subunit -N-terminal fragment [Tyr] -1-32 (P ~ (33)) significantly inhibited the progesterone secretion of rat luteal cells.In this study, the effect of P ~ (33) and other factors on the apoptosis of luteal cells was further investigated by using PMSG-hCG induced pseudo pregnancy model in rats.Under age rats Injected with 65IU of PMSG and injected with hCG50IU after 48h.On the fifth day of hCG injection, the cells were treated with P33 (40μg / P), P29 (37-65 amino acids) (50μg / only), oxytocin.OT (40μg / each) .Tyr (1.5mg / only) and E_2 (1.5mg / only) once daily: PGF_ (2α) (12.5μpg / only) The levels of plasma estrogen and progesterone in the ovaries treated with P, P ~ (33), P ~ (29), OT, PG_ (2α) and Tyr decreased, while the levels of plasma estrogen and progesterone (33) .P ~ (29) .OT, PGF (2α) and Tyr groups were directly extracted or incubated after nuclear incubation and extraction Of the low-molecular-weight DNA are increased.Instead of estrogen inhibition of low molecular weight (29), P (33), OT.PGF_ (2α) .Tyr and estrogen play an important role in the regulation of atrophy of the corpus luteum.P ~ (29), P ~ (33) ), OT.PGF_ (2α) .Tyr induced the expression of endonuclease mediated apoptosis in rat luteal cells and promoted the apoptosis of luteal cells; estrogen inhibited the apoptosis of luteal cells.This result is to further explore the apoptosis of luteal cells Mechanism laid the foundation.