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目的:观察人参二醇组皂苷(PDS)对感染性休克大鼠肝中血栓素B2(TXB2)及6-酮-前列腺素F1α(6-Keto-PGF1α)含量的影响,探讨其抗感染性休克的作用机制。方法:动物随机分为对照(Control)组;内毒素休克(LPS)组;地塞米松(LPS+Dex 2 mg.kg-1)组;人参二醇组皂苷(LPS+PDS)组。LPS+PDS组iv人参二醇组皂苷(22.5,45,90 mg.kg-1)葡萄糖溶液5mL.kg-1。10 min后iv细菌内毒素(LPS,5 mg.kg-1)复制感染性休克模型。颈动脉插管记录平均动脉压(MAP)。休克后4 h处死动物,称取肝20 mg匀浆后测TXB2和6-keto-PGF1α的含量。结果:注射内毒素后,LPS组的MAP迅速下降,在低水平维持,LPS+Dex组和LPS+PDS组的MAP未见明显下降;测得肝组织中TXB2和6-keto-PGF1α的含量在LPS+PDS中、大剂量组均显著低于LPS组,6-Keto-PGF1α/TXB2在中剂量组显著低于LPS组。结论:PDS可通过降低体内TXA2和PGI2的含量,调节血浆或组织中二者的平衡关系,改善内毒素休克大鼠的低血压状态,起到抗休克的作用。
Objective: To observe the effects of Panaxadiol Saponins (PDS) on the levels of TXB2 and 6-Keto-PGF1α in the liver of septic shock rats and to explore the protective effects of PDS against septic shock The mechanism of action. Methods: The animals were randomly divided into Control group, LPS group, LPS + Dex 2 mg.kg-1 group, and LPS + PDS group. The infectivity of iv bacterial endotoxin (LPS, 5 mg.kg-1) in LPS + PDS group iv after 5 mL.kg-1.10 min of glucose solution of ginseng diol saponin (22.5,45,90 mg.kg-1) Shock model. Carotid artery catheterization recorded mean arterial pressure (MAP). Animals were sacrificed 4 h after shock and the contents of TXB2 and 6-keto-PGF1α were measured after 20 mg of liver homogenate. Results: The MAP of LPS group decreased rapidly after injection of endotoxin. MAP at LPS + Dex group and LPS + PDS group decreased at low level. The content of TXB2 and 6-keto-PGF1α in LPS + LPS + PDS, high-dose group were significantly lower than the LPS group, 6-Keto-PGF1α / TXB2 in the middle dose group was significantly lower than the LPS group. Conclusion: PDS can reduce the level of TXA2 and PGI2 in vivo, regulate the balance between plasma and tissue, and improve the hypotensive state of endotoxic shock rats.