Edemann-Callesen Henriette, Bernhardt Nadine, Hlusicka Elizabeth Barroeta, Hintz Franziska, Habelt Bettina, Winter Rebecca, Neubert Isabell, Pelz Meike, Filla Alexandra, Soto-Montenegro Maria Luisa, Winter Christine, Hadar Ravit
Department of Psychiatry and Neuroscience, Campus Mitte, Charité University Medicine Berlin, Charitéplatz 1, 10117 Berlin, Germany.
Department of Psychiatry and Psychotherapy, Medical Faculty Carl Gustav Carus, Technische Universität, 01307 Dresden, Germany.
Antioxidants (Basel). 2023 May 9;12(5):1068. doi: 10.3390/antiox12051068.
Heightened levels of inflammation and oxidative stress are thought to be involved in the pathophysiology of schizophrenia. We aimed to assess whether intake of anti-inflammatory and anti-oxidant drugs during pregnancy prevents later schizophrenia-related outcomes in a neurodevelopmental rat model of this disorder.
Pregnant Wistar rats were injected with polyriboinosinic-polyribocytidilic acid (Poly I:C) or saline and subsequently treated with either N-acetyl cysteine (NAC) or omega-3 polyunsaturated fatty acids (PUFAs) until delivery. Controls rats received no treatment. In the offspring, neuroinflammation and anti-oxidant enzyme activity were assessed on postnatal day (PND) 21, 33, 48, and 90. Behavioral testing was performed at PND 90, followed by post-mortem neurochemical assessment and ex vivo MRI.
The supplement treatment led to a quicker restoration of the wellbeing of dams. In the adolescent Poly I:C offspring, the supplement treatment prevented an increase in microglial activity and partially prevented a deregulation in the anti-oxidant defense system. In the adult Poly I:C offspring, supplement treatment partially prevented dopamine deficits, which was paralleled by some changes in behavior. Exposure to omega-3 PUFAs prevented the enlargement of lateral ventricles.
Intake of over-the-counter supplements may assist in especially targeting the inflammatory response related to schizophrenia pathophysiology, aiding in diminishing later disease severity in the offspring.
炎症水平和氧化应激的升高被认为与精神分裂症的病理生理学有关。我们旨在评估孕期服用抗炎和抗氧化药物是否能预防这种疾病的神经发育大鼠模型中后来出现的精神分裂症相关结局。
给怀孕的Wistar大鼠注射聚肌苷酸-聚胞苷酸(Poly I:C)或生理盐水,随后用N-乙酰半胱氨酸(NAC)或ω-3多不饱和脂肪酸(PUFA)治疗至分娩。对照大鼠不接受治疗。在子代中,于出生后第(PND)21、33、48和90天评估神经炎症和抗氧化酶活性。在PND 90进行行为测试,随后进行死后神经化学评估和离体MRI。
补充治疗使母鼠的健康恢复得更快。在青春期的Poly I:C子代中,补充治疗可防止小胶质细胞活性增加,并部分防止抗氧化防御系统失调。在成年的Poly I:C子代中,补充治疗部分防止了多巴胺缺乏,这与行为上的一些变化平行。暴露于ω-3多不饱和脂肪酸可防止侧脑室扩大。
服用非处方补充剂可能有助于特别针对与精神分裂症病理生理学相关的炎症反应,有助于降低子代后期疾病的严重程度。