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经颅光生物调节(808纳米)通过抑制青春期前大鼠海马神经炎症、星形胶质细胞增生和小胶质细胞增生来减轻戊四氮诱导的癫痫发作。

Transcranial photobiomodulation (808 nm) attenuates pentylenetetrazole-induced seizures by suppressing hippocampal neuroinflammation, astrogliosis, and microgliosis in peripubertal rats.

作者信息

Tsai Chung-Min, Chang Shwu-Fen, Li Chih-Chuan, Chang Hsi

机构信息

Taipei Medical University, Graduate Institute of Medical Sciences, College of Medicine, Taipei, Taiwan.

MacKay Children's Hospital, Department of Pediatrics, Taipei, Taiwan.

出版信息

Neurophotonics. 2022 Jan;9(1):015006. doi: 10.1117/1.NPh.9.1.015006. Epub 2022 Mar 25.

Abstract

Transcranial photobiomodulation (tPBM) at 808 nm attenuates pentylenetetrazole (PTZ)-induced seizures and convulsive status epilepticus (CSE) in peripubertal rats by protecting neurons from injury and parvalbumin-positive interneurons from apoptosis, and preserving the integrity of perisomatic inhibitory networks. However, the effects of tPBM on neuroinflammation, astrogliosis, and microgliosis in epileptic rat brains are unknown. Thus, further study to unveil these aspects is needed for understanding the phenomena of tPBM on pediatric CSE prevention. To evaluate the effects of tPBM on neuroinflammation, astrogliosis, and microgliosis in peripubertal rat hippocampus with PTZ-induced seizures and SE. An 808-nm diode laser was applied transcranially to peripubertal rats prior to PTZ injection. Immunofluorescence staining of neuron-specific enolase (NSE) was used as a marker of neuroinflammation, glial fibrillary acid protein (GFAP) for astrogliosis, ionized calcium-binding adapter molecule 1 (Iba-1) for microgliosis, and mitochondrial cytochrome c oxidase subunit 1 (MT-CO1) for confirming the involvement of cytochrome c oxidase (CCO). tPBM significantly reduced NSE immunoreactivity in CA3 in PTZ-treated rats, GFAP immunoreactivity in CA1, and Iba-1 immunoreactivity in CA3. Enhancement of hippocampal MT-CO1 reflected that tPBM acted in CCO-dependent manner. tPBM (808) attenuated PTZ-induced seizures and SE by suppressing neuroinflammation, astrogliosis, and microgliosis in peripubertal rats.

摘要

808纳米的经颅光生物调节(tPBM)通过保护神经元免受损伤、保护小白蛋白阳性中间神经元免受凋亡以及维持躯体周围抑制网络的完整性,减轻了青春期前大鼠戊四氮(PTZ)诱导的癫痫发作和惊厥性癫痫持续状态(CSE)。然而,tPBM对癫痫大鼠大脑神经炎症、星形胶质细胞增生和小胶质细胞增生的影响尚不清楚。因此,需要进一步研究以揭示这些方面,从而理解tPBM预防小儿CSE的现象。为了评估tPBM对青春期前大鼠海马体中由PTZ诱导的癫痫发作和癫痫持续状态时神经炎症、星形胶质细胞增生和小胶质细胞增生的影响。在注射PTZ之前,将808纳米二极管激光经颅应用于青春期前大鼠。神经元特异性烯醇化酶(NSE)的免疫荧光染色用作神经炎症的标志物,胶质纤维酸性蛋白(GFAP)用于星形胶质细胞增生,离子钙结合衔接分子1(Iba-1)用于小胶质细胞增生,线粒体细胞色素c氧化酶亚基1(MT-CO1)用于确认细胞色素c氧化酶(CCO)的参与情况。tPBM显著降低了PTZ处理大鼠CA3区的NSE免疫反应性、CA1区的GFAP免疫反应性以及CA3区的Iba-1免疫反应性。海马体MT-CO1的增强反映出tPBM以CCO依赖的方式起作用。tPBM(808)通过抑制青春期前大鼠的神经炎症、星形胶质细胞增生和小胶质细胞增生,减轻了PTZ诱导的癫痫发作和癫痫持续状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cb8/8955735/5fddf7aa2953/NPh-009-015006-g001.jpg

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