Hu Xiaofang, Zhao Nan, Ranjbar Elham, Foruozandeh Hossein, Nahal Ali Seidkhani, Asadoola Yousef, Ahmadi Iraj
Department of Neurology, Shandong Public Health Clinical Center, Shandong University, Jinan, 250100, China.
Department of Neurosurgery, The First Hospital of Kunming (Affiliated Calmette Hospital of Kunming Medical University), Kunming, 650224, China.
Mol Biol Rep. 2024 Dec 20;52(1):67. doi: 10.1007/s11033-024-10165-9.
Oleuropein (OLE) has the potential to reduce oxidative stress and inflammation. So, in the present investigation, we explored the protective effect of OLE on brain aging induced by d-galactose (D-Gal) in a rat model.
40 Wister male adult rats were categorized into 5 groups. Group 1 received normal saline; group 2 was given 100 mg/kg of D-Gal intraperitoneally (IP). The rats in groups 3 to 5 were given D-Gal (100 mg/kg, IP) along with different doses of OLE (20, 40, and 80 mg/kg, respectively) orally. All administrations were performed daily for 8 weeks. 24 h after last treatment motor activity and memory impairment were evaluated. Then, the rats were euthanized and brain samples were collected for evaluating the levels of malondialdehyde (MDA), Brain-Derived Neurotrophic Factor (BDNF), protein carbonyl (PC), glutathione (GSH), glutathione peroxidase (GPX), catalase (CAT), Superoxide dismutase (SOD), Tumor necrosis factor alpha (TNF-α), interleukin 1 beta ( IL-1β), as well as Sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1) gene expression. The results showed that D-Gal significantly reduced motor activity and memory performance (P < 0.05). It also significantly reduced the GPX, CAT and SOD activities, GSH and BDNF levels as well as SIRT1 and PGC1 expression, and, significantly increased PC, MDA TNF-α and IL-1β levels in the brain tissue (P < 0.05). Administration of OLE restored all of the above parameters close to control group.
The findings demonstrated that OLE, through its antioxidant and anti-inflammatory properties, improved motor activity, memory impairment, and age-related neurological dysfunction.
橄榄苦苷（OLE）具有减轻氧化应激和炎症的潜力。因此，在本研究中，我们在大鼠模型中探究了OLE对D-半乳糖（D-Gal）诱导的脑衰老的保护作用。
40只成年雄性Wister大鼠被分为5组。第1组给予生理盐水；第2组腹腔注射100mg/kg D-Gal。第3至5组大鼠腹腔注射D-Gal（100mg/kg），并分别口服不同剂量的OLE（20、40和80mg/kg）。所有给药均每日进行，持续8周。最后一次治疗24小时后，评估运动活动和记忆损伤情况。然后，对大鼠实施安乐死并采集脑样本，以评估丙二醛（MDA）、脑源性神经营养因子（BDNF）、蛋白质羰基（PC）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPX）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、肿瘤坏死因子α（TNF-α）、白细胞介素1β（IL-1β）水平，以及沉默信息调节因子1（SIRT1）和过氧化物酶体增殖物激活受体γ共激活因子1α（PGC1）的基因表达。结果显示，D-Gal显著降低了运动活动和记忆表现（P<0.05）。它还显著降低了脑组织中的GPX、CAT和SOD活性、GSH和BDNF水平以及SIRT1和PGC1表达，并显著提高了PC、MDA、TNF-α和IL-1β水平（P<0.05）。给予OLE可使上述所有参数恢复至接近对照组的水平。
研究结果表明，OLE通过其抗氧化和抗炎特性，改善了运动活动、记忆损伤及与年龄相关的神经功能障碍。
