摘要
目的探讨人参皂苷Rbl对脑缺血再灌注损伤JAK2/STAT3胞内信号通路的影响,明确其保护机制。方法建立大脑中动脉缺血再灌注(MCAO/R)模型,将大鼠随机分为假手术组、溶媒组、人参皂苷Rbl低剂量组、人参皂苷Rb1高剂量组,观察大鼠神经行为学障碍程度,ELISA检测脑组织肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)的含量,免疫组织化学染色法观察缺血侧大脑p-JAK2和p-STAT3的表达。结果 (1)与溶媒组比较,人参皂苷Rbl高剂量组显著降低大鼠神经行为学评分(P<0.05)。(2)人参皂苷Rbl高剂量组明显减少TNF-α、IL-6的含量(P<0.05或P<0.01),而在低剂量组,TNF-α含量显著减少(P<0.05),IL-6的含量也有所降低但差异无统计学意义(P>0.05)。(3)人参皂苷Rbl高剂量组、低剂量组显著降低p-JAK2和p-STAT3的表达(P<0.05或P<0.01)。结论人参皂苷Rbl可能通过调控细胞因子介导的JAK2/STAT3信号途径保护脑缺血再灌注损伤。
Objective To explore the effect of ginsenoside Rb1on the JAK2/STAT3signal transduction pathway after cerebral ischemia-reperfusion in rats for identifying the protection mechanism.Methods Made the model of middle cerebral artery occlusion/reperfusion（MCAO/R）.Rats were randomly divided into sham group,vehicle group,high dosage group,and low dosage group of ginsenoside Rb1.The neurological deficit scores were assessed,the contents of TNF-αand IL-6in ischemia brain tissue were detected by ELISA and the expressions of p-JAK2and p-STAT3were observated in the cortex by immunohistochemisty staining.Results（1）The neurological deficit scores were significantly decreased in ginsenoside Rb1high dosage group compared with vehicle group（P〈0.05）.（2）Ginsenoside Rb1of high dosage significantly reduced the content of TNF-αand IL-6in ischemia brain tissue（P〈0.05or P〈0.01）,the content of TNF-αwas decreased significantly in low dosage group（P〈0.05）,the content of IL-6was also decreased but without statistical significance.（3）Both ginsenoside Rb1of low and high dosage reduced the expressions of pJAK2and p-STAT3after cerebral ischemia-reperfusion（P〈0.05or P〈0.01）.Conclusion Ginsenoside Rb1improved neurologic deficits′symptoms after cerebral ischemia-reperfusion,reduced the contents of TNF-αand IL-6and inhibited the phosphorylation of JAK2and STAT3.Therefore,Ginsenoside Rb1could protect cerebral ischemia-reperfusion injury by regulating the JAK2/STAT3 signal transduction pathway.
出处
《重庆医学》
CAS
CSCD
北大核心
2013年第17期1932-1934,共3页
Chongqing medicine
基金
泸州医学院青年基金资助项目(201125)
