摘要
【目的】探讨1-磷酸-神经鞘氨醇(S1P)对环磷酰胺(CTX)导致的大鼠卵巢功能损害的保护作用及可能机制。【方法】40只雌性SD大鼠随机分为4组,即实验对照组(生理盐水组)、CTX组、S1P+NS组及S1P+CTX组,每组10只,于结束用药的第1～2周内的动情间期处死,观察卵泡数量的变化,并采用半定量RT-PCR检测卵巢组织Bcl-2及Bax的mRNA变化。【结果】S1P+CTX组的原始卵泡、初级卵泡和生长卵泡数与S1P+NS组、对照组的差别不显著(P>0.05),而CTX组的所有卵泡数均少于其余3组,其差异均有显著性意义(P<0.01)。卵巢组织中,S1P两组Bcl-2 mRNA的表达明显高于对照组及CTX组(P<0.01),Bax mRNA表达明显低于对照组及CTX组(P<0.01);而CTX组的Bcl-2 mRNA表达明显低于对照组及S1P两组(P<0.01),BaxmRNA表达明显高于对照组及及S1P两组(P<0.01)。【结论】S1P能预防CTX导致的大鼠卵巢功能损害,其抗凋亡作用可能是通过调节Bcl-2家族成员表达而实现。
[Objective] To study the effect of sphingosine-l-phosphate （SIP） against cyelophosphamide （CTX） induced gonadotoxicity in female rats. [ Methods ] Forty SD female rats were divided randomly into four groups ： contrel （received normal saline（NS）, CTX, SIP＋NS, SIP＋CTX respectively. AU rats were killed between the first and the second week in the diestrus stage after stopping medicines to compare the number of the primordial follicles, the primary foUieles and the growth foUicles. The expression of the Bel-2 and Bax mRNA in the ovaries were examined by the RT-PCR. [Results] The number of primordial follicles, primary follicles and growth follicles in the SIP＋CTX group was close to that in the control group and the S1P＋NS group （P 〉0.05）.But the number of all kinds of follicles was decreasing in the CTX group, and there were significant differences between that of these groups（P 〈 0.01 ）.The levels of the Bcl-2 mRNA in the two SIP groups were significantly higher than that in the CTX group and the control group, but levels of the Bax mRNA were on the contrary （P 〈 0.01）. The level of the Bcl-2 mRNA in the CTX group was significantly lower than that in the SIP groups and the control group, but the level of the Bax mRNA was on the contrary （P 〈 0.01）. [Conclusion] SIP could reduce the cyclophospham/de-induced ovar/an damage in rats, and the role of its against apoptosis might through reguhting the expression of the Bcl-2 and Bax mRNA in the ovary.
出处
《中山大学学报（医学科学版）》
CAS
CSCD
北大核心
2007年第1期15-18,39,共5页
Journal of Sun Yat-Sen University:Medical Sciences
基金
卫生部部属(管)医疗机构2004-2006临床学科重点项目(卫规财发〈2004〉468号)
国家教育部博士点基金资助项目(20050558093)
