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目的观察丹参素对新生大鼠缺氧缺血性脑损伤脑组织SOD、MDA的影响及探讨丹参素的脑损伤保护作用机理。方法 7日龄SD新生大鼠78只,随机分成5组:假手术组(n=6);缺氧缺血模型组(n=18);丹参素低剂量组(n=18);丹参素中剂量组(n=18);丹参素高剂量组(n=18)。通过结扎左颈总动脉和吸入8%低氧混合气制备缺氧缺血性脑损伤(HIBD)动物模型。假手术组不进行缺氧缺血处理。丹参素各治疗组按低、中、高剂量分别于造模后0、24h两个时点按15mg/kg、30mg/kg、60mg/kg腹腔注射用生理盐水稀释至0.5ml的丹参素注射液。缺氧缺血模型组及假手术组于相应时点腹腔注射生理盐水0.5ml。假手术组于缺氧缺血后6h,HIBD组与各丹参素组于缺氧缺血后6h、24h、48h断头取脑,测定脑组织匀浆SOD、MDA。结果与假手术组比较,缺氧缺血模型组新生大鼠大脑中MDA水平升高,SOD活性降低;应用丹参素治疗后MDA水平回降,SOD活性回升,且呈剂量效应。差异有统计学意义(P<0.05)。结论丹参素有减轻新生大鼠缺血再灌注时氧自由基引起的氧化损伤作用,从而发挥脑保护作用。
Objective To observe the effects of Danshensu on the expression of SOD and MDA in brain tissue of neonatal rats with hypoxic-ischemic brain damage and to explore the protective mechanism of Danshensu. Methods Totally 78 SD neonatal rats of 7 days old were randomly divided into 5 groups: sham operation group (n = 6), hypoxia-ischemia model group (n = 18), Danshensu low dose group Medium dose group (n = 18); high dose of danshensu group (n = 18). Animal model of hypoxic-ischemic brain damage (HIBD) was established by ligating the left common carotid artery and inhaling 8% hypoxia mixture. Sham-operated group did not undergo hypoxic-ischemic treatment. Danshensu treatment groups according to low, medium and high doses were 0,24 h after modeling at two time points by 15mg / kg, 30mg / kg, 60mg / kg intraperitoneal injection with saline diluted to 0.5ml of Danshensu injection . Hypoxic-ischemic model group and sham-operated group were intraperitoneally injected with 0.5 ml normal saline at the corresponding time point. Sham operation group at 6h after hypoxia-ischemia, HIBD group and Danshensu group hypoxia-ischemia 6h, 24h, 48h after decapitation brain, determination of SOD and MDA in brain homogenates. Results Compared with the sham-operation group, the MDA level in the brain of hypoxic-ischemic model group was decreased and the activity of SOD was decreased. The level of MDA dropped back and the activity of SOD rose after Danshensu treatment. The difference was statistically significant (P <0.05). Conclusion Danshensu can alleviate the oxidative damage caused by oxygen free radicals during the process of ischemia-reperfusion in neonatal rats, and thus exert cerebral protection.