摘要
Objective： Inflammatory reactions induced by microglia in the brain play an important part in the pathogenesis of focal cerebral ischemia/reperfusion （I/R） injury, resulting in neuronal death. Salvianolate Lyophilized Injection （SLI） and Xueshuantong Injection （Lyophilized） （XST）, which have been widely used in the treatment of acutely cerebral infarction clinically in China, exhibit various biological activities. In this study, the neuroprotective properties of SLI combined with XST in a rat model of middle cerebral artery occlusion- reperfusion （MCAO/R） were investigated. Methods： In this study, male Wistar rats were subjected to 1.5h of middle cerebral artery occlusion followed by reperfusion for 24 h. The rats were randomly divided into the following six groups： normal group （NOR）, model group （MOD）, SLI group （21 mg/kg, SLI）, ）（ST group （100 mg/kg, ）（ST）, SLI combined with XST （XST 100 mg/kg ＋ SLI 21 mg/kg, 1X1S）, and Edaravone （as a positive control drug, 6 mL/kg, EDI）, once a day for 3 d. The neuronal injury, the expression of glial fibrillary acidic protein （GFAP） and ionized calcium binding adaptor molecule 1 （IBA-1）, and the changes of pro-inflammatory mediators interleukin- 6 （IL-6）, tumor necrosis factor alpha （TNF-α） and anti-inflammatory mediator interleukin-10 （IL-10） were observed. Results： 1X1S treatment significantly increased the number of neuron, compared with the MOD group, SH group and XST group. Gliosis （GFAP and IBA-1） and expression of pro-inflammatory mediators IL-6 and TNF-a were significantly reduced. Meanwhile, 1XIS significantly increased the expression of anti- inflammatory mediator IL-10 in the brains of MCAO/R rats, compared with the MOD group, SLI and XST groups. SLI and XST also remarkably down-regulated the expression of IL-6 and TNF-α compared with the MOD group. Conclusions： This study shows that SLI combined with XST （1X1S） can protect cerebral ischemia- reperfusion injury due to its anti-inflammatory property, and may provide a potential promising new therapeutic strategy for acute ischemic stroke.
Objective： Inflammatory reactions induced by microglia in the brain play an important part in the pathogenesis of focal cerebral ischemia/reperfusion （I/R） injury, resulting in neuronal death. Salvianolate Lyophilized Injection （SLI） and Xueshuantong Injection （Lyophilized） （XST）, which have been widely used in the treatment of acutely cerebral infarction clinically in China, exhibit various biological activities. In this study, the neuroprotective properties of SLI combined with XST in a rat model of middle cerebral artery occlusion- reperfusion （MCAO/R） were investigated. Methods： In this study, male Wistar rats were subjected to 1.5h of middle cerebral artery occlusion followed by reperfusion for 24 h. The rats were randomly divided into the following six groups： normal group （NOR）, model group （MOD）, SLI group （21 mg/kg, SLI）, ）（ST group （100 mg/kg, ）（ST）, SLI combined with XST （XST 100 mg/kg ＋ SLI 21 mg/kg, 1X1S）, and Edaravone （as a positive control drug, 6 mL/kg, EDI）, once a day for 3 d. The neuronal injury, the expression of glial fibrillary acidic protein （GFAP） and ionized calcium binding adaptor molecule 1 （IBA-1）, and the changes of pro-inflammatory mediators interleukin- 6 （IL-6）, tumor necrosis factor alpha （TNF-α） and anti-inflammatory mediator interleukin-10 （IL-10） were observed. Results： 1X1S treatment significantly increased the number of neuron, compared with the MOD group, SH group and XST group. Gliosis （GFAP and IBA-1） and expression of pro-inflammatory mediators IL-6 and TNF-a were significantly reduced. Meanwhile, 1XIS significantly increased the expression of anti- inflammatory mediator IL-10 in the brains of MCAO/R rats, compared with the MOD group, SLI and XST groups. SLI and XST also remarkably down-regulated the expression of IL-6 and TNF-α compared with the MOD group. Conclusions： This study shows that SLI combined with XST （1X1S） can protect cerebral ischemia- reperfusion injury due to its anti-inflammatory property, and may provide a potential promising new therapeutic strategy for acute ischemic stroke.
作者
fu-jiang wang
zuo-yan sun
rui-lin li
li-min hu
li-juan chai
shao-xia wang
hong guo
yue zhang
Fu-jiang Wanga,b, Zuo-yan Suna,b, Rui-lin Lia,b, Li-min HUb, Li-juan Chaib, Shao-xia Wanga, Hong Guob, Yue Zhang(a. Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China; b. Key Laboratory of Formula of Traditional Chinese Medicine, Ministry of Education, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, Chin)
基金
financially supported by the National Natural Science Foundation (81573644)
the Natural Science Foundation of Tianjin (14JCYBJC28900)
the Tianjin Technology Innovation System and the Condition of Platform Construction Plan (16PTSYJC00120)
