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Procyanidin B2 mitigates behavioral impairment and protects myelin integrity in cuprizone-induced schizophrenia in mice

机译:原花青素B2减轻行为障碍并保护铜吡酮诱导的精神分裂症小鼠的髓磷脂完整性

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Numerous studies have suggested that neuropathological changes in schizophrenia may be related to damage to white matter or demyelination. Procyanidin B2, which is a constituent of many fruits such as grapes and strawberries, has various biological activities such as anti-inflammatory and anti-tumor activity, as has been reported. This study aimed to estimate the effects of procyanidin B2 on behavioral impairment and the protection of myelin integrity in a cuprizone-induced schizophrenia model. Mice were exposed to cuprizone (0.2% w/w in chow) for five weeks to induce schizophrenia-like behavioral changes and demyelination. Procyanidin B2 (20 or 100 mg kg ~(?1) day ~(?1) ) or vehicle was administered orally to mice after withdrawal from cuprizone. Behavioral impairment was detected with an open-field test, a rotarod test and a Morris water maze. Myelin integrity was assessed using LFB staining and MBP expression, including immunofluorescence and western blotting. In addition, enhancements in the expression of HO-1 and NQO1 suggested that procyanidin B2 may regulate oxidative homeostasis via promoting the translation of Nrf2 to the nucleus. Data indicated that procyanidin B2 could mitigate behavioral impairment and protect myelin integrity in the cuprizone-induced model via regulating oxidative stress by activating Nrf2 signaling.
机译:大量研究表明,精神分裂症的神经病理学改变可能与白质损伤或脱髓鞘有关。如前所述,原花青素B2是许多水果(例如葡萄和草莓)的成分,具有多种生物活性,例如抗炎和抗肿瘤活性。这项研究旨在评估在花椒酮诱导的精神分裂症模型中原花青素B2对行为障碍的影响和对髓鞘完整性的保护。将小鼠暴露于铜酮(浓度为食物的0.2%w / w)中五周,以诱导精神分裂症样行为改变和脱髓鞘。从铜酮中止后,对小鼠口服原花青素B2(20或100 mg kg〜(?1)天〜(?1))或媒介物。通过开放视野测试,旋转脚架测试和莫里斯水迷宫检测到行为障碍。使用LFB染色和MBP表达(包括免疫荧光和蛋白质印迹)评估髓磷脂的完整性。此外,HO-1和NQO1表达的增强表明原花青素B2可能通过促进Nrf2向核的翻译来调节氧化稳态。数据表明,原花青素B2可以通过激活Nrf2信号传导来调节氧化应激,从而减轻铜质酮诱导的模型中的行为障碍并保护髓鞘完整性。

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