探讨绝经前、后健康女性线粒体功能变化及雌激素抗衰老的线粒体机制。

2008年3月至9月，选取绝经前、后健康女性共计41例，按是否绝经将其分为未绝经组(n＝15)和绝经组(n＝26) (研究遵循程序符合中山大学附属第三医院负责人体试验委员会制定的伦理学标准，得到该委员会批准，且分组征得受试者知情同意)。比较两组血小板线粒体相对膜电位差(mitochondrial membrane potential，ΔΨm)及三磷酸腺苷(ATP)。并将绝经组血小板线粒体标本分为2份，其中一份血小板线粒体用苯甲酸雌二醇(estrogen benzoate，EB)孵育1 h(绝经＋雌激素组)，比较孵育前、后线粒体膜电位差及三磷酸腺苷水平变化。

未绝经组和绝经组线粒体相对膜电位差分别为1.59±0.29和1.30±0.17；三磷酸腺苷水平分别为(3.38±0.67)μg/mL和(1.60±0.97)μg/mL，两组比较，差异有显著意义(P<0.05)。绝经组肘静脉血标本经苯甲酸雌二醇孵育1 h后(绝经＋雌激素组)，线粒体相对膜电位差及三磷酸腺苷水平显著增加，与绝经组孵育前比较，差异有显著意义(P<0.05)。

女性绝经后线粒体功能减退，绝经后加速衰老的机制可能与雌激素撤退导致线粒体功能障碍有关，雌激素可通过保护线粒体功能从而发挥抗衰老作用。

To investigate functional changes of mitochondria in pre- and post-menopausal healthy women and anti-aging mechanism of estrogen on the mitochondria.

From March to September 2008, 41 pre- and post-menopausal healthy women were selected in this study, and they were divided into 2 groups, pre-menopausal group (n=15) and post-menopausal group (n=26). Informed consent was obtained from all participates. Mitochondrial membrane potential (ΔΨm) and adenosine triphosphate of platelets (ATP) were compared between 2 groups. As for post-menopausal group, thrombocytic mitochondria were incubated with estradiol benzoate (EB) for 1 hour (post-menopausal+ estrogen group), and then changes of mitochondrial membrane potential and adenosine triphosphate in mitochondria were compared before and after incubation.

Mitochondrial membrane potential were 1.59±0.29 and 1.30±0.17 in pre-menopausal group and post-menopausal group, respectively and adenosine triphosphate were (3.38±0.67) μg/mL and (1.60±0.97) μg/mL, respectively, which had significant difference (P<0.05). After estrogen treatment, mitochondrial membrane potential and adenosine triphosphate increased significantly, and the difference was significant compared with post-menopausal group with out estrogen treatment (P<0.05).

The mechanism of accelerated aging after menopause may be related to estrogen withdraw, which leads to mitochondrial dysfunction. Therefore, estrogen may play a role in anti-aging through protecting mitochondrial function.