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作 者:吴岚[1] 周素娴[1] 刘开祥[1] 俸军林[1]
出 处:《时珍国医国药》2010年第3期527-529,共3页Lishizhen Medicine and Materia Medica Research
基 金:广西自然科学基金(No.0848015);广西卫生厅科研课题基金资助(Z2008262)
摘 要:目的探讨青藤碱(sinomenine,Sin)对糖尿病大鼠脑缺血再灌注损伤单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子-α(TNF-α)含量的影响。方法采用高脂高糖饮食加腹腔注射小剂量链脲霉素建立糖尿病大鼠模型,造模成功后将大鼠随机分为假手术组、缺血再灌注组、Sin低剂量治疗组和Sin高剂量治疗组。线栓法建立局灶性脑缺血再灌注模型。Sin低(30 mg/kg)、高剂量(60 mg/kg)治疗组于术前30 min分别给予大鼠腹腔注射。采用酶联免疫吸附实验(ELISA)法检测缺血90 min再灌注24 h大鼠额顶部皮质MCP-1和TNF-α含量的变化,并进行2,3,5-三苯基氯化四氮唑(TTC)染色和HE染色观察脑梗塞体积及病理形态学变化。结果①脑缺血再灌注24h,缺血再灌注组MCP-1和TNF-α含量明显升高,与假手术组比较,差异具有显著性(均P<0.05);与缺血再灌注组比较,Sin高、低剂量治疗组均显著减少MCP-1和TNF-α含量;高、低剂量组之间差异亦具有显著性(P<0.05);②Sin治疗组脑梗塞体积较缺血再灌注组减小,高、低剂量组之间差异亦具有显著性(P<0.05);③Sin高、低剂量治疗组脑组织缺血损伤病理学改变明显轻于缺血再灌注组,Sin高剂量治疗组缺血改变亦轻于低剂量治疗组。结论Sin对糖尿病大鼠缺血再灌注脑损伤具有保护作用,其机制可能与降低缺血再灌注损伤脑组织MCP-1和TNF-α含量,抑制再灌注损伤炎症反应有关。Objective To study the effect of sinomenine(Sin) on the contents of MCP-1 and TNF-α after cerebral ischemia reperfusion(I/R) injury in diabetic rats.Methods In this experiment,rat model of diabetes mellitus was made by high sucrose,fat diet and streptozotion injection.Diabetic rats were randomly divided into 4 groups,namely sham operated group,I/R group,low dose Sin treated group and high dose Sin treated group.The focal middle cerebral artery occlusion(MCAO) model was made by suture-occluded method.Sin were given intraperitoneally to rats 30min before focal cerebral ischemia operation.After 90min MCAO following 24h of reperfusion,we investigated the contents of MCP-1 and TNF-α in ischemic frontal and parietal cortex.HE staining and TTC staining were also investigated.Results ①Compared with sham operated group,the contents of MCP-1 and TNF-α were increased at 24h of reperfusion in the ischemic territory(P0.05).Compared with I/R group,Sin dose-dependently reduced the contents of MCP-1 and TNF-α(all P0.05).②Compared with I/R group,cerebral infarction volume in low and high dose Sin treated groups was decreased dose-dependently(all P0.05).③The change of ischemic impairment in low or high dose Sin treated group was lighter than that of I/R group,and high dose Sin treated group was lighter than that of low dose Sin treated group.Conclusion Sin may reduced cerebral ischemia-reperfusion injury by decreasing the contents of MCP-1 and TNF-α in diabetic rats.
关 键 词:缺血再灌注 单核细胞趋化蛋白-1 肿瘤坏死因子-α 青藤碱
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