Kiray Muge, Ergur Bekir Ugur, Bagriyanik Alper, Pekcetin Cetin, Aksu Ilkay, Buldan Zisan
Department of Histology, Dokuz Eylul University Medical School, Balcova, Izmir 35340, Turkey.
Acta Histochem. 2007;109(6):480-5. doi: 10.1016/j.acthis.2007.04.008. Epub 2007 Aug 14.
Aging is accompanied by significant structural and functional transformations of all organs and systems. Age-associated increase in apoptotic behavior may cause disease. Older cells are more susceptible to endogenous oxidative damage, and oxidative stress is a potent inducer of apoptosis. Deprenyl is an irreversible monoamine-oxidase B inhibitor which has anti-oxidant, anti-apoptotic and neuroprotective effects. Estrogen is also a neuroprotective and anti-oxidant hormone. The objectives of this study were to determine whether the anti-oxidative effects of deprenyl can suppress apoptotic activity, with or without estradiol, in aged female rat livers. In this study, ovariectomized female Wistar albino rats were divided into six groups as follows; young (3 months old) saline-treated control, aged (24 months old) saline-treated control, aged deprenyl treated, aged estradiol treated, aged deprenyl plus estradiol treated and aged sham controls. All rats except for the sham group were treated for 21 days. Determination of oxidative stress parameters was performed spectrophotometrically. To detect apoptotic cells, TUNEL staining was performed. The results were analyzed by one-way ANOVA post hoc Bonferroni test. Deprenyl and estradiol administration, alone or in combination, decreased significantly the levels of lipid peroxidation and increased superoxide dismutase activity in the liver relative to aged control and sham rats (P<0.05). The number of TUNEL positive cells decreased significantly in deprenyl and estradiol-treated rats compared with aged control and sham rats. The results indicate that deprenyl treatment alone, or in combination with estradiol, may modulate age-related apoptotic changes in rat liver by decreasing oxidative stress.
衰老伴随着所有器官和系统显著的结构和功能转变。与年龄相关的凋亡行为增加可能会引发疾病。衰老细胞更容易受到内源性氧化损伤，而氧化应激是凋亡的强效诱导剂。司来吉兰是一种不可逆的单胺氧化酶B抑制剂，具有抗氧化、抗凋亡和神经保护作用。雌激素也是一种具有神经保护和抗氧化作用的激素。本研究的目的是确定司来吉兰的抗氧化作用是否能在有或没有雌二醇的情况下抑制老年雌性大鼠肝脏中的凋亡活性。在本研究中，将去卵巢的雌性Wistar白化大鼠分为以下六组：年轻（3个月大）生理盐水处理对照组、老年（24个月大）生理盐水处理对照组、老年司来吉兰处理组、老年雌二醇处理组、老年司来吉兰加雌二醇处理组和老年假手术对照组。除假手术组外，所有大鼠均接受21天的处理。采用分光光度法测定氧化应激参数。为了检测凋亡细胞，进行了TUNEL染色。结果采用单因素方差分析后的Bonferroni检验进行分析。与老年对照组和假手术组大鼠相比，单独或联合给予司来吉兰和雌二醇可显著降低肝脏中的脂质过氧化水平，并增加超氧化物歧化酶活性（P<0.05）。与老年对照组和假手术组大鼠相比，司来吉兰和雌二醇处理组大鼠中TUNEL阳性细胞数量显著减少。结果表明，单独使用司来吉兰或与雌二醇联合使用，可能通过降低氧化应激来调节大鼠肝脏中与年龄相关的凋亡变化。
