栀子苷阻抑脑缺血损伤级联反应的作用环节探讨

目的 :观察持久性局灶性脑缺血损伤大鼠脑组织TNF-α ,IL-1β及血浆vWF、血清NSE含量的变化 ,探讨栀子苷阻抑脑缺血损伤级联反应的作用环节。方法 :成年雄性SD大鼠 ,随机分成假手术对照组、模型组、栀子苷组、三七总皂苷组。使用血管腔内尼龙线栓塞术造成大鼠持久性大脑中动脉栓塞 (PMCAO) ,制作缺血 12 ,24h的局灶性脑缺血模型 ,应用放射免疫法 (RIA)检测脑组织匀浆TNF-α和IL-1β含量与血清NSE含量 ,应用酶联吸附免疫法 (ELISA)检测血浆vWF含量。结果 :缺血 12h与缺血 24h ,伴随脑组织TNF-α ,IL-1β含量升高 ,血浆vWF、血清NSE含量呈现同步的升高。栀子苷可以明显阻抑缺血 12h和 24h脑组织TNF-α和IL-1β含量升高 ,还可阻抑缺血 12h和 24h血浆vWF含量的升高 ,但对缺血 12h和 24h血清NSE含量无明显影响。结论 :栀子苷可阻抑脑缺血损伤后致炎因子TNF-α和IL-1β及血浆vWF的表达 ,显示出其抗缺血后血管内皮细胞损伤、在炎症病理环节阻抑脑缺血损伤级联反应的作用。

Protective effect of jasminoidin on cascade of damage of cerebral ischemia in rats

OBJECTIVE: To study the protective effect of jasminoidin on cascade of damage of cerebral ischemia. METHOD: The rats were randomly divided into four groups: sham-operated group, ischemic group, the jasminoidin-treatment group and PNS-treatment group. Focal cerebral ischemia was produced by permanent occlusion of left middle cerebral artery (PMCAO) in rats. Radioimmunoassay (RIA) was utilized to identify the content of tumor necrosis factor-alpha (TNF-alpha) and interlukin 1beta (IL-1beta) in brain tissue of rats following ischemia. and that of Neuron-specific enolase (NSE) in rat's serum was observed too. The plasma concentration of vonWillebrand factor (vWF) was identified by enzyme-linked immunoadsordent assay (ELISA). RESULT: After 12 h and 24 h of ischemia, the contents of TNF-alpha and IL-1beta and vWF as well as on NSE showed concomitant increase. Jasminoidin dramatically inhibited the increase of TNF-alpha and IL-1beta after 12 h and 24 h of ischemia, and repressed the increase of vWF after 12 h and 24 h of ischemia too. However, the influence of jasminodin NSE after 12 h and 24 h of ischemia was not significant. CONCLUSION: Jasminoidin had good effect on repressing the expression of TNF-alpha and IL-1beta as well as vWF caused by cerebral ischemia, thus it manifested the effect of relieving the damage to vascular endothelial cell and blocking the progress of cascade damage of cerebral ischemia through inhibiting the process of inflammation.