Liu Yichen, Li Weiguang, Hu Linyan, Liu Ying, Li Baoquan, Sun Changqing, Zhang Chenggang, Zou Liping
Department of Pediatrics, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, P.R. China.
Beijing Institute of Radiation Medicine, State Key Laboratory of Proteomics, Cognitive and Mental Health Research Center of PLA, Beijing 100850, P.R. China.
Mol Med Rep. 2015 Feb;11(2):837-42. doi: 10.3892/mmr.2014.2879. Epub 2014 Nov 6.
The present study aimed to investigate the role of nitric oxide (NO) against perinatal hypoxic‑ischemic brain damage (HIBD) in rats by electroacupuncture (EA) and to examine its potential neuroprotective mechanism. NO content, the number of positive cells, neuronal nitric oxide synthase (nNOS) and nuclear factor‑κB (NF‑κB) in rat cortex cells were determined. The results demonstrated that treatment with EA significantly downregulated the NO content in the cortex cells (*P<0.05, **P<0.01, compared with the control groups) and alleviated cell damage in the cortex of rats with HIBD. The activator, S‑adenosyl‑L‑methionine and the inhibitor, hydroxylamine of cystathionine‑β‑synthase (CBS), aggravated and remitted the hypoxic damage in the cortex cells, respectively. In addition, treatment with EA significantly downregulated the expression of nNOS and NF‑κB in the rat cortex cells (*P<0.05, **P<0.01, compared with the control groups). The results also indicated that treatment with EA downregulated the NO content of cortical cells against HIBD via the NF‑κB/nNOS pathway and further implied that the hydrogen sulfide/CBS system may be involved in the process. The present study provided a significant reference for the prevention and treatment of HIBD using the EA technique and also described a novel protective mechanism.
本研究旨在通过电针（EA）探讨一氧化氮（NO）对大鼠围产期缺氧缺血性脑损伤（HIBD）的作用，并研究其潜在的神经保护机制。测定大鼠皮质细胞中NO含量、阳性细胞数量、神经元型一氧化氮合酶（nNOS）和核因子-κB（NF-κB）。结果表明，与对照组相比，电针治疗显著下调了皮质细胞中的NO含量（*P<0.05，**P<0.01），并减轻了HIBD大鼠皮质中的细胞损伤。胱硫醚-β-合酶（CBS）的激活剂S-腺苷-L-甲硫氨酸和抑制剂羟胺分别加重和减轻了皮质细胞中的缺氧损伤。此外，与对照组相比，电针治疗显著下调了大鼠皮质细胞中nNOS和NF-κB的表达（*P<0.05，**P<0.01）。结果还表明，电针治疗通过NF-κB/nNOS途径下调了HIBD大鼠皮质细胞中的NO含量，进一步提示硫化氢/CBS系统可能参与了这一过程。本研究为应用电针技术防治HIBD提供了重要参考，并阐述了一种新的保护机制。
