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Neurotoxicity in pre-eclampsia involves oxidative injury, exacerbated cholinergic activity and impaired proteolytic and purinergic activities in cortex and cerebellum.
Human & Experimental Toxicology ( IF 2.8 ) Pub Date : 2020-08-10 , DOI: 10.1177/0960327120946477
O K Ijomone 1, 2 , O L Erukainure 3 , P Shallie 4 , T Naicker 1
Affiliation  

Women with a history of pre-eclampsia (PE) tend to have a higher risk of developing cardiovascular and neurological diseases later in life. Imbalance in oxidative markers and purinergic enzymes have been implicated in the pathogenesis of neurological disease. This study investigated the effect of PE on oxidative imbalance, purinergic enzyme inhibitory activity, acetylcholinesterase and chymotrypsin activities in the brain of PE rat model at post-partum/post-natal day (PP/PND) 60. Pregnant rats divided into early-onset and late-onset groups were administered with Nω-nitro-l-arginine methyl through drinking water at gestational days 8–17. Rats were allowed free access to water throughout the pregnancy and allowed to deliver on their own. The mother and the pups were euthanized at PP and PND 60, respectively, the cortex and the cerebellum excised, homogenized and stored for analyses of the enzymes. Results showed an increase in nitric oxide and malondialdehyde with a concomitant decrease in reduced glutathione and superoxide dismutase, an indication of oxidative damage. Also, there was an increase in acetylcholinesterase activity with a decrease in chymotrypsin, adenylpyrophosphatase and ecto-nucleoside triphosphate diphosphohydrolase activities in both the cortex and the cerebellum of the mother and the pups at PND 60. These results indicate the involvement of oxidative stress, increased cholinergic activity and depleted proteolytic and purinergic activities in PE-induced neurotoxicity.



中文翻译:

先兆子痫的神经毒性包括氧化损伤、加剧的胆碱能活性以及皮质和小脑的蛋白水解和嘌呤能活性受损。

有先兆子痫 (PE) 病史的女性在晚年患心血管和神经系统疾病的风险更高。氧化标记物和嘌呤能酶的不平衡与神经疾病的发病机制有关。本研究探讨PE对产后/产后日(PP/PND) 60 PE大鼠模型脑内氧化失衡、嘌呤能酶抑制活性、乙酰胆碱酯酶和胰凝乳蛋白酶活性的影响。 妊娠大鼠分为早发型和晚发型组给予N ω-硝基-l- 精氨酸甲基通过在妊娠 8-17 天喝水。允许大鼠在整个怀孕期间自由饮水并允许其自行分娩。母亲和幼崽分别在 PP 和 PND 60 时被安乐死,皮层和小脑被切除、匀浆并储存用于酶分析。结果显示一氧化氮和丙二醛增加,同时还原型谷胱甘肽和超氧化物歧化酶减少,这是氧化损伤的迹象。此外,在 PND 60 时,母亲和幼崽的皮质和小脑中的乙酰胆碱酯酶活性增加,糜蛋白酶、腺苷焦磷酸酶和外核苷三磷酸二磷酸水解酶活性降低。这些结果表明氧化应激的参与,

更新日期:2020-08-10
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