| 郭 超,卞 涛,卜 伟,马善波,段佳林,王艳华,文爱东.毛蕊异黄酮通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤的研究[J].,2019,19(4):631-635 |
| 毛蕊异黄酮通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤的研究 |
| Calycosin Exerts Neuroprotective Effect on Cerebral Ischemia/Reperfusion Injury through Inhibiting Calpain-1 Expression |
| 投稿时间：2018-06-30 修订日期：2018-07-26 |
| DOI：10.13241/j.cnki.pmb.2019.04.006 |
| 中文关键词: 毛蕊异黄酮 脑缺血 卡配因 作用机制 |
| 英文关键词: Calycosin Cerebral Ischemia Calpain-1 Mechanism |
| 基金项目:国家自然科学基金项目(81403134) |
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| 中文摘要: |
| 摘要 目的：探讨毛蕊异黄酮抗脑缺血再灌注损伤的作用是否与抑制calpain-1的表达有关。方法：将SD大鼠随机分为假手术组、模型组以及药物组，采用线栓法建立大鼠大脑中动脉阻断(MCAO)模型，于缺血再灌注前30 min腹腔注射给予20 mg/kg毛蕊异黄酮或等体积的溶剂。再灌注24 h后，行神经功能学评分、脑梗死面积以及神经元凋亡检测；再灌注12 h、24 h时，采用免疫组化和蛋白印迹技术检测大鼠脑皮层calpain-1的表达。结果：与假手术组大鼠比较，MCAO模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率及calpain-1的表达均明显升高(P＜0.05)，而毛蕊异黄酮能够降低模型组大鼠再灌注24 h后神经功能学评分、梗死面积、神经元凋亡率以及calpain-1的表达(P＜0.05)。结论：毛蕊异黄酮可能通过抑制calpain-1的表达发挥抗脑缺血再灌注损伤作用。 |
| 英文摘要: |
| ABSTRACT Objective: To explore whether calpain-1 was involved in the protective effect of calycosin against cerebral ischemia/ reperfusion injury. Methods: Rats were randomly allocated to sham-operated, middle cerebral artery occlusion (MCAO) model and caly- cosin groups. MCAO model was made by suture-occluded method. At 30 min before ischemia/reperfusion, rats were injected intraperi- toneally with 20 mg/kg calycosin and the same volume of resolver. The neurologic score, infarct area and neuronal apoptosis were mea- sured at 24 h after ischemia/reperfusion. At 12 h and 24 h after ischemia/reperfusion, the calpain-1 protein expression of cerebral cortex were detected by immunohistochemical and western blot. Results: The neurologic score, infarct area, the number of TUNEL positive neurons and the level of calpain-1 of MCAO model group were obviously increased compared with those of the sham group at 24 h after reperfusion (P<0.05). However, the calycosin was significantlydecreased the elevation of these biological markers in MCAO model group after 24 h reperfusion(P<0.05). Conclusion: Calycosin exerted neuroprotective effect on cerebral ischemia/reperfusion injury through in- hibiting calpain-1 expression. |
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