人参皂苷Rg1对DSS诱导溃疡性结肠炎小鼠凝血功能的调节作用

Ginsenoside-Rg1regulates blood coagulation in DSS-induced colitis mice

[目的]探讨中药三七有效成分人参皂苷Rg1治疗溃疡性结肠炎(UC)的可能机制。[方法]采用5%葡聚糖硫酸钠(DSS)建立UC小鼠模型,将小鼠随机分为人参皂苷Rg1高剂量组、人参皂苷Rg1低剂量组、美沙拉嗪肠溶片(5-ASA)组、模型1组、模型2组和正常组(每组10只)。模型1组于造模7d处死,其余各组于造模第7天开始灌胃给药,连续给药7d处死。小鼠眼球采血检测凝血酶原时间(PT)、活化部分凝血酶时间(APTT)、凝血酶时间(TT);放免法检测血浆中血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)含量。[结果]与正常组相比,模型1组及模型2组PT、APTT、TT明显缩短(P<0.01),血浆TXB2明显升高(P<0.01),6-keto-PGF1α降低(P<0.01),TXB2/6-keto-PGF1α比值升高(P<0.01);人参皂苷Rg1高剂量组、人参皂苷Rg1低剂量组、5-ASA组经用药干预后,PT、APTT、TT均有不同程度的延长,血浆TXB2水平降低、6-keto-PGF1α表达增加,与模型1组和模型2组比较差异有统计学意义(P<0.01)。[结论]人参皂苷Rg1可延长出凝血时间,下调血浆TXB2水平,上调6-keto-PGF1α含量,缓解UC小鼠的血液高凝状态,改善机体微循环,从而抑制或降低炎症反应的扩大,以达到缓解UC的症状作用。

[Objective]To investigate the possible mechanisms underlying the therapeutic effect of active ingredient of Radix Notoginseng（Ginsenoside-Rgl ） on ulcerative colitis （UC）. [Methods] Experimental colitis was induced in mice by oral dextran sulfate sodium （DSS） administration. Mice were randomized in to 6 groups：Rgl high-dose group, Rgl low-dose group, 5-ASA group, model 1 group, model 2 group and normal group （each n=10）. Model 1 were sacrificed after 7 days of DSS,while others were intervened by corresponding drugs （oral garage） for 7 days,and then sacrifice was applied. Blood was collected from the peri-orbital venous sinus for blood coagulation analysis, and TXB2 ＆ 6-keto-PGF1α determination （by radio- immunoassay）. [Results] Prothrombin time （PT）, activated partial thromboplastin time （APTT） and thrombin time （TT） in both model groups were significantly shorter than that in the normal group （P〈 0.01）. Plasma TXB2 was markedly increased （P%0.01）, and plasma 6-keto-PGF1α was significantly de creased （P^0.01） in the model groups compared to the normal group. After the treatments, statistically significant improvement was found for PT, APTT and TT in all treating groups, compared to Model 1 group （P%0.01）;and plasma TXB2 ＆ 6-keto-PGF1α levels were improved in all treating groups compared to both Model 1 and 2 groups （P〈0.01）. EConclusion] Ginsenoside-Rgl restricted inflammation progress via improving hypercoagulability and microcirculation by PT, APTT, TT, TXB2 and 6-keto-PGF1α regula-tions.