右美托咪定对大鼠肺缺血再灌注引起的氧化应激损伤的保护作用

发布时间：2018-04-28 16:36

本文选题：右美托咪定预处理 + 肺氧化应激损伤　；参考：《中国临床药理学杂志》2017年13期

【摘要】：目的研究右美托咪定预处理对大鼠肺缺血再灌注引起的氧化应激的影响。方法用夹闭左肺门45 min后放开的方法建立肺缺血再灌注损伤模型。按照随机数字表法将SD大鼠随机分为假手术组、模型组和实验组,每组8只。假手术组仅左侧开胸,无任何处理;动物于夹闭前通过股静脉,实验组给予右美托咪定(3.0μg·kg~(-1)·h~(-1)),模型组给予同体积的0.9%Na Cl,均60 min。再灌注120 min后,采集左肺静脉中的血样进行血气分析;通过HE染色进行肺损伤评分(LIS);通过黄嘌呤氧化酶法、硫代巴比妥酸法分别检测左肺组织超氧化物岐化酶(SOD)、丙二醛(MDA)含量;通过免疫印迹法检测核因子E2相关因子(Nrf2)蛋白表达。结果与假手术组的LIS为3.5±0.6、MDA为(1.6±0.3)nmol·mg~(-1)相比,模型组LIS为8.5±1.3和MDA为(5.8±2.2)nmol·mg~(-1),模型组水平明显升高,差异均有统计学意义(均P0.05)。与假手术组的SOD活性为(65.1±4.8)U·mg~(-1),模型组的SOD活性为(30.3±4.1)U·mg~(-1),显著降低,差异有统计学意义(P0.05)。与模型组相比,实验组的LIS为5.0±1.2和MDA水平为(2.7±0.3)nmol·mg~(-1),显著降低;而SOD活性为(61.4±1.9)U·mg~(-1),显著升高,差异均有统计学意义(均P0.05)。与假手术组的细胞核Nrf2蛋白表达为0.25±0.04相比,模型组的表达为0.12±0.02,差异有统计学意义(P0.05);与模型组相比,实验组的Nrf2蛋白表达为0.53±0.05,差异有统计学意义(P0.05)。结论用右美托咪定预处理,可以激活Nrf2通路,降低MDA水平而上调SOD活性,减轻肺缺血再灌注大鼠的氧化应激损伤并改善肺功能。
[Abstract]:Aim to study the effect of dexmetomidine preconditioning on oxidative stress induced by lung ischemia reperfusion in rats. Methods Pulmonary ischemia-reperfusion injury model was established by releasing left hilum after 45 min clamping. Sprague-Dawley rats were randomly divided into sham-operated group, model group and experimental group with 8 rats in each group. In the sham operation group, the left thoracotomy was only left without any treatment, and the experimental group was given dexmetomidine 3.0 渭 g 路kg ~ (-1) 路h ~ (-1) by femoral vein before clamping, and the model group was given the same volume of 0.9%Na _ 1 for 60 min. After reperfusion for 120 min, blood samples from left pulmonary vein were collected for blood gas analysis, lung injury scores were evaluated by HE staining, contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in left lung tissue were detected by xanthine oxidase method and thiobarbituric acid method respectively. The expression of nuclear factor E 2 related factor nrf2) was detected by Western blot. Results compared with the sham-operated group, the LIS of the model group was 8.5 卤1.3 and the MDA of the model group was 5.8 卤2.2)nmol. The level of LIS in the model group was significantly higher than that in the model group (P 0.05). The activity of SOD was 65.1 卤4.8U mg / L in the model group and 30.3 卤4.1U / mg / L in the model group, which was significantly lower than that in the sham group (P 0.05). Compared with the model group, the levels of LIS and MDA in the experimental group were 5.0 卤1.2 and 2.7 卤0.3)nmol / mg-1, significantly lower, while the activity of SOD was 61.4 卤1.9 U / mg / L, which was significantly higher than that in the control group (P < 0.05). The expression of nuclear Nrf2 protein in the model group was 0.12 卤0.02 compared with that in the sham operation group (0.25 卤0.04), the difference was statistically significant (P 0.05), and the expression of Nrf2 protein in the experimental group was 0.53 卤0.05 (P 0.05) compared with the model group (P 0.05). Conclusion preconditioning with dexmetidine can activate the Nrf2 pathway, decrease the level of MDA and up-regulate the activity of SOD, alleviate oxidative stress injury and improve lung function in rats with pulmonary ischemia-reperfusion injury.
【作者单位】：滨州医学院附属医院麻醉科;滨州医学院附属医院生殖医学中心;
【分类号】：R965

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