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目的:观察参姜锁阳益气片对寒凝气滞血瘀证大鼠血清中6-酮-前列腺素F1a(6-ketoPGF1a)、血栓素B2(TXB2)及氧自由基代谢的影响。方法:将SD大鼠随机分为正常组,模型组,试药(参姜锁阳益气片)高、中、低剂量组和中药(大株红景天胶囊)对照组。除正常组外,其余组采用肾上腺素加冰水浴复合低温冷冻法建立大鼠寒凝气滞血瘀证模型,各组ig给药。正常组及模型组ig给予等量生理盐水,每日1次,连续2周。给药结束后,放射免疫法检测血清中6-keto-PGF1a、TXB2含量,化学比色法检测血清中一氧化氮合酶(NOS)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性。结果:与模型组比较,参姜锁阳益气片低、中、高剂量组均能显著降低血清中6-keto-PGF1a、TXB2含量(P<0.01);中、高剂量组SOD、GSH-Px活性明显升高(P<0.05,P<0.01),高剂量组血清中NOS活性升高(P<0.05)。结论:参姜锁阳益气片可以调控寒凝气滞血瘀证大鼠血液中6-keto-PGF1a、TXB2水平并能改善模型大鼠氧自由基代谢,这可能是其预防和治疗高寒环境下脏腑器官功能减退的作用机制之一。
Objective: To observe the effect of ginseng Cynomorium yingguiqi tablet on the metabolism of 6-keto-PGF1a, TXB2 and oxygen free radicals in rats with cold-stagnation and blood stasis syndrome. Methods: The SD rats were randomly divided into normal group, model group, high dose group, middle dose group and low dose dose group (Ginseng Cynomorii Yisi Qi Tablet) and control group of traditional Chinese medicine (Dazhong Rhodiola Capsule). In addition to the normal group, the rest of the group using epinephrine combined with ice-water bath compound cryogenic freezing cold stasis syndrome model rats, each group ig administration. Normal group and model group ig given the same amount of saline once a day for 2 weeks. After administration, the content of 6-keto-PGF1a and TXB2 in serum was detected by radioimmunoassay and the levels of nitric oxide synthase (NOS), superoxide dismutase (SOD) and glutathione Oxidase (GSH-Px) activity. Results: Compared with the model group, the levels of 6-keto-PGF1a and TXB2 in the low, medium and high doses of Ginger Decoction group were significantly decreased (P <0.01); the activities of SOD and GSH-Px (P <0.05, P <0.01). The activity of NOS in high dose group increased (P <0.05). Conclusion: Ginseng Cynomorium Yisiqi tablet can regulate the level of 6-keto-PGF1a and TXB2 in the blood of rats with cold stasis qi stagnation and blood stasis and can improve the metabolism of oxygen free radicals in the model rats, which may be the prevention and treatment of viscera in alpine environment One of the mechanisms of organ dysfunction.