胆酸、栀子苷配伍对脑缺血时脑组织TNF-α、IL-1β和ICAM-1含量的影响

Effects of Cholic Acid and Jasminoidin on the Levels of Cerebral TNF-α, IL-1 β and ICAM-1 in the Rats Undergone Cerebral Ischemia

目的 观察胆酸、栀子苷及两者配伍对持久性局灶性脑缺血损伤大鼠脑组织中肿瘤坏死因子 α(TNF α)、白细胞介素 1β(IL 1β)、细胞间粘附分子 1(ICAM 1)以及血清神经元特异性烯醇化酶(NSE)含量的影响 ,探讨胆酸、栀子苷阻抑脑缺血炎症级联损伤的作用环节及配伍作用特征。方法 成年雄性SD大鼠 ,随机分成假手术对照组、模型组、胆酸组、栀子苷组、胆酸和栀子苷配伍组、血栓通组。线栓法复制大鼠持久性大脑中动脉栓塞 (PMCAO) 12、2 4h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与血清NSE含量 ,酶联免疫吸附法 (ELISA)检测脑组织匀浆ICAM 1含量。结果 缺血 12h与 2 4h ,大鼠脑组织TNF α、IL 1β、ICAM 1以及血清NSE含量有不同程度的升高。胆酸、栀子苷可以明显阻抑缺血 12h和 2 4h脑组织TNF α和IL 1β的增加 ,胆酸还可阻抑缺血 12h血清NSE含量的增加 ,但两者对脑组织ICAM 1含量与缺血 2 4h血清NSE含量无明显影响。而胆酸和栀子苷配伍不仅明显阻抑缺血 12h和 2 4h脑组织TNF α、IL 1β含量的增加 ,而且对缺血 12h和 2 4h脑组织ICAM 1含量及缺血 12h血清NSE含量增加也呈现了显著的阻抑作用。结论 胆酸。

Objective To observe the effects of cholic acid and jasminoidin in combination on the levels of cerebral TNF-α, IL-1 β, ICAM-1 and serum NSE in the rats with persistent focal cerebral ischemia, in order to investigate the links at which cholic acid and jasminoidin act to inhibit the cascade of the cerebral ischemic inflammatory injury and to investigate the mechanism of the effects produced by cholic acid and jasminoidin in combination. Methods Adult male SD rats were randomly divided into the sham operation group, model group, cholic acid group, jasminoidin group, cholic acid plus jasminoidin group, and Xueshuantong group. The rat model of focal cerebral ischemia was induced by persistent middle cerebral artery occlusion for 12 and 14 hours, respectively, by a thread ligation method. RIA was used to detect the levels of TNF-α and IL-1 β in the cerebral homogenate and the level of NSE in the serum. ELISA was used to detect the level of ICAM-1 in the cerebral homogenate. Results The levels of TNF-α, IL-1 β, ICAM-1 and NSE were found increased to different degrees, respectively, under cerebral ischemia for both 12 and 24 hours. Both cholic acid and jasminoidin could markedly inhibit the increase of TNF-α and IL-1 β under both the 12-hour and 24-hour cerebral ischemia; in addition, cholic acid could also inhibit the increase of NSE under the 12-hour cerebral ischemia; but both cholic acid and jasminoidin showed no obvious effects on the levels of ICAM-1 and of NSE under the 24-hour cerebral ischemia. However, the coadministration of cholic acid and jasminoidin could not only markedly inhibit the decrease of TNF-α and IL-1 β under both the 12-hour and 24-hour cerebral ischemia, but also markedly inhibit the increase of ICAM-1 under both the 12-hour and 24-hour cerebral ischemia and the increase of NSE under 12-hour cerebral ischemia. Conclusion Cholic acid and jasminoidin and their coadministration possess good effects for repressing the expressions of inflammatory cytokines and adhesive molecules under cerebral ischemia, hence reducing the inflammatory injury. The coadministration of cholic acid and jasminoidin shows particularly good effects for interfering the inflammatory process at different times and different links and for repressing the cascade of the inflammatory injury due to cerebral ischemia, hence inhibiting the damage to neurons.