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机构地区:[1]湖北省十堰市太和医院,湖北医药学院附属医院,湖北十堰442000 [2]湖北医药学院,湖北十堰442000
出 处:《中国中医急症》2016年第8期1515-1517,共3页Journal of Emergency in Traditional Chinese Medicine
基 金:湖北省十堰市科技局资助课题(ZD2013003)
摘 要:目的观察丹参提取液对缺血再灌注模型大鼠子宫的影响,为临床研究子宫缺血再灌注损伤的防治提供理论依据。方法 SD大鼠36只,采用线栓法建立大鼠子宫缺血再灌注损伤模型,在术前连续7 d用丹参提取液灌胃进行干预并设为丹参组,另设假手术组和模型组作对照。检测术后24 h大鼠子宫组织白介素-2(IL-2)、丙二醛(MDA)、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)浓度,免疫组织化学法检测子宫组织中Bcl-2和Bax蛋白表达。结果与模型组比较,丹参组大鼠子宫组织中Bax蛋白表达、IL-2和MDA显著降低(P<0.05),而SOD活性、Bc1-2蛋白表达显著提高(P<0.05)。结论丹参提取液对大鼠子宫缺血再灌注损伤有保护作用,其作用机制可能与其下调Bax蛋白、提高SOD活性、抑制自由基对缺血再灌子宫组织的破坏、降低IL-2造成的炎症反应有关。Objective:To establish uterine ischemia reperfusion injury model of rat,and to observe the effect of Chinese herbal medicine Salvia miltiorrhiza extract on the uterus of rats with ischemia reperfusion injury to provide theoretical basis for clinical study of the prevention and treatment of uterine ischemia reperfusion injury.Methods:Uterine ischemia reperfusion injury model of 36 SD rats was established with thread embolism method,before operation receiving Salvia miltiorrhiza extract intragastric administration to intervene for 7 days as Danshen group.Sham operation group and the model group were used as control.The levels of IL-2,malondialdehyde(MDA),total superoxide dismutase(SOD) and lactate dehydrogenase(LDH) were detected in 24 hours after operation,and the expression of Bc1-2 and Bax in uterine tissues was detected by immunohistochemistry.Results:Compared with the model group,Bax protein expression,IL-2 and MDA in the rat's uterine tissue of Salvia miltiorrhiza group decreased significantly(P 0.05),and SOD activity and Bcl-2 protein expression increased significantly(P 0.05).Conclusion:Salvia miltiorrhiza can Huoxue has the effects of blood circulation,regulating menstruation,removing blood stasis and anti-inflammatory and a protective effect on uterine ischemia/reperfusion injury in rats,whose mechanism may be related to reducing Bax protein,increasing the activity of SOD,inhibition of free radicals on ischemia reperfusion of uterine tissue damage and decreasing IL-2 caused by inflammation.
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