Effects of prenatal photobiomodulation treatment on neonatal hypoxic ischemia in rat offspring.

Effects of prenatal photobiomodulation treatment on neonatal hypoxic ischemia in rat offspring.
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产前光生物调节治疗对大鼠后代新生儿缺氧缺血的影响。

DOI:
10.7150/thno.49672
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发表时间:
2021
期刊:
影响因子:
12.4
通讯作者:
Zhang Q
Zhang Q
中科院分区:
医学1区
文献类型:
--
作者:
Yang L;Dong Y;Wu C;Youngblood H;Li Y;Zong X;Li L;Xu T;Zhang Q

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新生儿缺氧缺血性损伤(HI)是一种严重的并发症,常导致新生儿死亡和儿童长期神经行为缺陷。目前,新生儿HI损伤的唯一治疗选择是治疗性低温。然而,必要的专门设备,可能的不良副作用,以及有限的有效性,这种疗法创造了迫切需要开发新的HI治疗方法。光生物调节(PBM)已被证明是对多种大脑疾病的动物模型,以及有限的人类研究的神经保护。然而,PBM治疗对新生儿HI损伤的影响尚不清楚。研究方法:从妊娠第1天(GD1)至GD21,每周三次在妊娠大鼠腹部施加两分钟PBM(808 nm连续波激光,新生儿脑上为8 mW/cm 2)。新生儿右颈总动脉结扎后,皮质和海马相关的行为缺陷,由于HI侮辱使用一组行为测试。然后评估HI损伤和PBM预处理对梗死面积、突触、树突和白色物质损伤、神经元变性、细胞凋亡、线粒体功能、线粒体碎片化、氧化应激和神经胶质增生的影响。结果:产前PBM治疗可显著提高新生大鼠的存活率,并减少HI后的梗死面积。行为测试显示,产前PBM治疗显着减轻皮质相关的运动缺陷和海马相关的记忆和学习功能障碍。此外,在用PBM处理的HI动物中,线粒体功能和完整性得到保护。其他研究表明,产前PBM治疗显着减轻HI诱导的神经炎症,氧化应激,和骨髓细胞/星形胶质细胞活化。结论:产前PBM对新生HI大鼠具有神经保护作用。这种神经保护的潜在机制可能包括线粒体功能的保护、炎症的减少和氧化应激的降低。我们的研究结果支持可能使用PBM治疗高危妊娠,以减轻或预防HI诱导的脑损伤在围产期。
Neonatal hypoxic-ischemic (HI) injury is a severe complication often leading to neonatal death and long-term neurobehavioral deficits in children. Currently, the only treatment option available for neonatal HI injury is therapeutic hypothermia. However, the necessary specialized equipment, possible adverse side effects, and limited effectiveness of this therapy creates an urgent need for the development of new HI treatment methods. Photobiomodulation (PBM) has been shown to be neuroprotective against multiple brain disorders in animal models, as well as limited human studies. However, the effects of PBM treatment on neonatal HI injury remain unclear. Methods: Two-minutes PBM (808 nm continuous wave laser, 8 mW/cm2 on neonatal brain) was applied three times weekly on the abdomen of pregnant rats from gestation day 1 (GD1) to GD21. After neonatal right common carotid artery ligation, cortex- and hippocampus-related behavioral deficits due to HI insult were measured using a battery of behavioral tests. The effects of HI insult and PBM pretreatment on infarct size; synaptic, dendritic, and white matter damage; neuronal degeneration; apoptosis; mitochondrial function; mitochondrial fragmentation; oxidative stress; and gliosis were then assessed. Results: Prenatal PBM treatment significantly improved the survival rate of neonatal rats and decreased infarct size after HI insult. Behavioral tests revealed that prenatal PBM treatment significantly alleviated cortex-related motor deficits and hippocampus-related memory and learning dysfunction. In addition, mitochondrial function and integrity were protected in HI animals treated with PBM. Additional studies revealed that prenatal PBM treatment significantly alleviated HI-induced neuroinflammation, oxidative stress, and myeloid cell/astrocyte activation. Conclusion: Prenatal PBM treatment exerts neuroprotective effects on neonatal HI rats. Underlying mechanisms for this neuroprotection may include preservation of mitochondrial function, reduction of inflammation, and decreased oxidative stress. Our findings support the possible use of PBM treatment in high-risk pregnancies to alleviate or prevent HI-induced brain injury in the perinatal period.
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