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西蒙胶囊促血小板生成与长毒研究
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摘要
研究背景
     血小板减少性紫癜为常见病、多发病,该病的发病机制主要为自身免疫机制失调,临床表现为外周血小板减少。目前,该病的药物治疗为皮质类固醇激素和免疫抑制剂,但长期应用不良反应较多,且停药后易复发。西蒙为旋花科甘薯属植物,巴西民间证明,西蒙薯块具有止血作用。西蒙胶囊是用西蒙干叶提取物制成,本实验对西蒙胶囊升血小板作用及安全性进行了研究。
     方法
     家兔注射豚鼠抗兔血小板血清诱发免疫性血小板减少症模型;大鼠注射兔抗大鼠血小板血清建立大免疫性血小板减少症动物模型;辐照小鼠致血小板减少模型;家兔注射花生四烯酸诱导血小板减少症模型。血小板、红细胞、白细胞、巨核细胞计数;比色法测定血红蛋白,血小板用酶联免疫吸附法(ELISA)测定血小板相关抗体IgG(PAIgG)。
     在体犬与大鼠观察了其长期毒性。
     结果
     结果显示,在注射豚鼠抗兔血小板血清引起的家兔免疫性血小板减少模型,3个剂量(分别为0.23、0.46、0.92g/kg)的西蒙胶囊预防或治疗给药均能升高血小板,降低巨核细胞数和PAIgG水平。在注射兔抗大鼠血小板血清引起大鼠免疫性血小板减少模型,西蒙胶囊(剂量分别为0.44、0.88、1.76g/kg)能显著升高血小板,但不影响红细胞和白细胞数。在辐照小鼠所致的血小板减少模型,西蒙胶囊(剂量分别为0.64、1.27、2.55g/kg)能显著升高血小板,也能升高白细胞数、血红蛋白水平;在家兔注射花生四烯酸诱导血小板减少模型,西蒙胶囊(剂量分别为0.23g、0.46、0.92g/kg)能升高血小板和白细胞数。
     在体大鼠灌胃给予西蒙胶囊(4.90、2.45、1.22g/kg·d),连续13周和恢复期,血液细胞学、血液生化学、器官形态学无明显病理学改变。同样,在体Beagle犬灌胃西蒙(3.50、1.75、0.88g/kg·d),连续26周和恢复期,血液细胞学、血液生化学、器官形态学也无明显病理学改变。
     结论
     在免疫、辐身或化学药物所致血小板减少模型,西蒙胶囊能显著升高血小板数。
     在体动物(大鼠、犬)长期给予西蒙胶囊,未见明显毒性作用。
Background
     Thrombocytopenia is a common and frequently occurring disease, which is thought to be related to the autoimmune disorder, and with clinical symptom of decreased platelet count in peripheral blood. Classic treatment of thrombocytopenia is through drugs like glucocorticoids or immunosuppressor, but the adverse effects caused by the long-term usage of those drugs are quite common, and the disease recrudescence frequently happens after medicine withdrawn. Simon belongs to Ipomoea category of Convolvulaceae section, and the traditional usage of simon in Brazil has proved its effect on hemostasis. In the present study, we explored the effect of simon capsules on elevating platelet count and evaluated the safety of the drug.
     METHODS
     Immune thrombocytopenia rabbit model was induced by injection of guinea pig serum of anti-rabbit-platelet in rabbits. Immune thrombocytopenia rat model was induced by injection of rabbit serum of anti-rat-platelet in rats. Thrombocytopenia mouse model was induced by radiation in mice. Thrombocytopenia rabbit model was induced by injection of arachidonic acid in rabbits. Platelets, red blood cells, white blood cells and megakaryoblastic cells were counted, hemoglobin was measured through colorimetric method, and platelet related IgG (PAIgG) were measured through ELISA method.
     Long-term toxicology of Simon capsules was evaluated in bothdogs and rats.
     RESULTS
     Pretreatment or treatment with simon capsules increased platelets, while decreased megakaryoblastic cells and PAIgG level in the immune thrombocytopenia rabbit model. In the immune thrombocytopenia rat model, simon capsules significantly increased platelets count, but had no effect on red blood cells and white blood cells. In the thrombocytopenia mouse model, simon capsules significantly increased platelets count, and elevated white blood cells and hemoglobin level. In the thrombocytopenia rabbit model, simon capsules increased platelets and white blood cells.
     In rats and Beagle dogs, orally administration of simon capsules didn't induce obvious pathologic changes in routine blood count, biochemistry blood analysis and organic morphology for the continuing 13 weeks treatment and during the recovery period.
     CONCLUSION
     Simon capsules significantly increase platelet count in thrombocytopenia models induced by immune response, radiation or chemical compounds.
     Long-term treatment with simon capsules does not induce obvious toxicology effects.
引文
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