摘要
目的探讨芍药苷(PF)对缺氧缺血性脑损伤(HIBD)新生大鼠脑组织丙二醛(MDA)、超氧化物歧化酶(SOD)的影响及其脑保护作用机制。方法7日龄SD新生大鼠78只,随机分为5组:假手术组(n=6),HIBD模型组(n=18),PF低剂量组(n=18),PF中剂量组(n=18),PF高剂量组(n=18)。通过结扎左颈总动脉和吸入80mL/L氧气和920mL/L氮气2h制备HIBD动物模型。假手术组不进行缺氧缺血处理。各PF治疗组按低、中、高剂量分别于造模0、24h按5、10、20mg/kgPF,计算每只新生鼠用药量后,吸取医用无菌9g/L盐水溶解配制成1g/L的PF注射液,加9g/L盐水稀释至0.5mL,腹腔注射。HIBD模型组及假手术组于相应时点腹腔注射9g/L盐水0.5mL。假手术组分离左颈总动脉后6h,HIBD模型组与各PF组于缺氧缺血后6、24、48h断头取脑,测定其脑组织匀浆SOD、MDA水平。结果缺氧缺血新生大鼠脑组织MDA水平较假手术组升高,且随着时间延长进一步升高;而应用PF治疗后其水平较HIBD组回降,且呈一定的剂量效应,差异有统计学意义(Pa<0.05)。大脑组织SOD活性较假手术组降低,随着时间延长而进一步降低;应用PF治疗后其活性较HIBD组回升,呈一定的剂量效应,差异有统计学意义(Pa<0.05)。结论PF能减轻新生大鼠HIBD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 explore the effects of paeoniflorin(PF)on malondlaldehyde(MDA) and superoxide dismutase(SOD) levels in neonatal rats with hypoxic-ischemic brain damage(HIBD) and the neuroprotective effect of paeoniflorin against HIBD in neonatal rats.Methods Seventy-eight seven-day-old Sprague-Dawley(SD) neonatal rats were randomly divided into 5 groups.Sham operation group(n=6) were treated with normal sodium injection by intraperitoneal injection 0 h after operation.HIBD models group(n=18) were treated with normal sodium injection by intraperitoneal injection 0,24 h after hypoxic ischemic(HI).PF 5 mg/kg group(n=18),PF 10 mg/kg group(n=18) and PF 20 mg/kg group(n=18) were treated with both normal sodium injection and PF 5 mg/kg,PF 10 mg/kg and PF 20 mg/kg respectively by intraperitoneal injection 0,24 h after HI.HIBD rats were established by ligating the left common carotid artery,followed by exposure to 80 mL/L oxygen and 920 mL/L nitrogen for 2 h in the HIBD model group and all the PF groups.The sham operation group was not subjected to HI.The neonatal rats in sham operation group were sacrificed 6 h after operation.Another neonatal rats in HIBD model group,PF 5 mg/kg group,PF 10 mg/kg group and PF 20 mg/kg group were sacrificed 6,24,48 h after HI and the levels of MDA,SOD in the brain were assessed.Results Compared with those of sham operation group,the level of MDA in HIBD model group significantly increased and the level of SOD decreased with the time prolonged(Pa〈0.05).Compared with those of HIBD model group,with the time prolonged,the levels of MDA in PF 5 mg/kg group,PF 10 mg/kg group and PF 20 mg/kg group were significantly reduced and the level of SOD elevated with the dose-effect relation(Pa〈0.05).Conclusions PF can promote the level of SOD and cut down the level of MDA in the brain of neonatal rats with HIBD,so it can prevent brain against HIBD by inhibiting the release of free radicals.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2008年第16期1272-1273,1279,共3页
Journal of Applied Clinical Pediatrics
关键词
缺氧缺血性脑损伤
芍药苷
超氧化物歧化酶
丙二醛
大鼠
新生
hypoxic-ischemic brain damage
paeoniflorin
superoxide dismutase
malondlaldehyde
neonatal rat