Xue Jing, Zhang Xiangjian, Zhang Cong, Kang Ning, Liu Xiaoxia, Yu Jingying, Zhang Nan, Wang Hong, Zhang Lan, Chen Rong, Cui Lili, Wang Lina, Wang Xiaolu
Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China.
Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, PR China; Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, Hebei 050000, PR China; Hebei Key Laboratory of Vascular Homeostasis, Shijiazhuang, Hebei, 050000, PR China.
J Ethnopharmacol. 2016 Apr 22;182:181-9. doi: 10.1016/j.jep.2016.02.022. Epub 2016 Feb 20.
Naoxintong (NXT), a renowned traditional Chinese medicine in China, has been used for the treatment of acute and chronic cardio-cerebrovascular diseases in clinic for more than 20 years.
To evaluate the potential neuroprotective effect of NXT against ischemia reperfusion (I/R) injury in mice and investigate the underlying mechanisms.
Focal cerebral I/R injury in adult male CD-1 mice was induced by transient middle cerebral artery occlusion (tMCAO) for 1h followed by reperfusion for 23h. Mice were randomly divided into five groups: Sham group; tMCAO group; Vehicle group; NXT-treated groups at doses of 0.36g/kg and 0.54g/kg. The effects of NXT on murine neurological function were estimated by neurological defect scores, infarct volume and brain water content at 24h after tMCAO. Immunohistochemistry and Western blot were used to detect the expression of LOX-1, pERK1/2 and NF-κB at 24h after tMCAO. qRT-PCR was used to detect the expression of LOX-1 and NF-κB at 24h after tMCAO.
Compared with Vehicle group, 0.54g/kg group of NXT significantly ameliorated neurological outcome, infarction volume and brain water content, decreased the expression of LOX-1, pERK1/2 and NF-κB (P<0.05).
NXT protected the mice brain against I/R injury, and this protection maybe associated with the down-regulation of LOX-1, pERK1/2 and NF-κB expression.
脑心通（NXT）是中国一种著名的传统中药，已在临床上用于治疗急慢性心脑血管疾病20多年。
评估脑心通对小鼠缺血再灌注（I/R）损伤的潜在神经保护作用，并探讨其潜在机制。
成年雄性CD-1小鼠通过短暂大脑中动脉闭塞（tMCAO）1小时，然后再灌注23小时诱导局灶性脑I/R损伤。小鼠随机分为五组：假手术组；tMCAO组；溶剂组；0.36g/kg和0.54g/kg剂量的脑心通治疗组。在tMCAO后24小时，通过神经功能缺损评分、梗死体积和脑含水量评估脑心通对小鼠神经功能的影响。免疫组织化学和蛋白质印迹法用于检测tMCAO后24小时LOX-1、pERK1/2和NF-κB的表达。qRT-PCR用于检测tMCAO后24小时LOX-1和NF-κB的表达。
与溶剂组相比，0.54g/kg剂量的脑心通组显著改善了神经功能结局、梗死体积和脑含水量，降低了LOX-1、pERK1/2和NF-κB的表达（P<0.05）。
脑心通对小鼠脑I/R损伤具有保护作用，这种保护作用可能与下调LOX-1、pERK1/2和NF-κB的表达有关。
