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目的:研究血竭对UC急性期大鼠血浆TXB2和β-TG表达的影响,评价血竭在治疗UC过程中抑制血小板活化的有效性。方法:60只SD大鼠,雌雄各半,随机分成5组,空白组给予自由饮食,模型对照组及低、中、高浓度血竭治疗组给予3%DSS溶液自由饮用7天,制造UC急性期模型。造模成功后,空白组、模型对照组给予生理盐水灌胃,低、中、高浓度血竭治疗组给予不同浓度的血竭混悬液4ml/只灌胃,治疗7天。观察疾病活动指数(DAI)、血浆TXB2及β-TG表达。结果:低、中、高浓度血竭治疗组各组DAI指数及血浆TXB2表达均与对照组比较有统计学意义(P<0.01);中浓度和高浓度血竭治疗组血浆β-TG含量与对照组相比较有统计学意义(P<0.05)。结论:血竭能够一定程度的抑制DSS诱导的UC模型中血小板活化,降低血小板活化引起的一系列炎症反应。
OBJECTIVE: To study the effect of DRG on the expression of TXB2 and β-TG in the plasma of acute UC rats, and to evaluate the effectiveness of DRX in inhibiting platelet activation during the treatment of UC. Methods: Sixty male and female SD rats were randomly divided into five groups. The rats in the blank group were given free diet. The rats in the model control group and the low, middle and high concentration blood serum treatment groups were given 7% DSS solution freely for 7 days to make UC acute Period model. After the model was established successfully, the blank group and the model control group were given normal saline. The low, medium and high concentration blood serum treatment groups were given different concentrations of blood serum suspension 4ml / only for 7 days. Disease activity index (DAI), plasma TXB2 and β-TG expression were observed. Results: Compared with the control group, DAI index and plasma TXB2 expression in each group of low, medium and high concentration of blood serum treatment group were statistically significant (P <0.01); and plasma concentration of β-TG and The control group was statistically significant (P <0.05). Conclusion: DRG can inhibit platelet activation in DSS-induced UC model to a certain extent and reduce a series of inflammatory reaction caused by platelet activation.