原花青素对局灶性脑缺血大鼠脑组织SOD、MDA和NF-κB的影响_临床医学论文.docVIP

原花青素对局灶性脑缺血大鼠脑组织SOD、MDA和NF-κB的影响_临床医学论文 原花青素对局灶性脑缺血大鼠脑组织SOD、MDA和NF-κB的影响_临床医学论文 作者：刘畅 张萍 闵连秋 贾玉洁，刘学文 【摘要】 　　目的 探讨原花青素(Procyanidins，PC)对局灶性脑缺血大鼠神经细胞保护作用及其机制。方法 随机将大鼠均分为假手术组、模型组、PC-1组(50 mg/kg)、PC-2组(100 mg/kg)和PC-3组(200 mg/kg )。以线栓法制备持续性局灶性脑缺血模型，24 h后断头取脑制备组织匀浆测超氧化物歧化酶(superoxide dismutase，SOD)、丙二醛(malondialdehyde，MDA)及用免疫组化SABC法，统计大鼠海马CA1区每高倍镜视野NF-κB阳性表达率［阳性细胞数/(阳性细胞数+阴性细胞数)×100%］。结果 ①超氧化物歧化酶：PC能明显增强脑组织中超氧化物歧化酶活性，与模型组比较有显著差异［ (50.55±5.87) (U/mg prot)、(51.44±7.06) (U/mg prot)、(55.32±6.39) (U/mg prot)、(39.28±5.67) (U/mg prot)，0.01］。②丙二醛含量：PC能明显降低丙二醛含量，与模型组比较有显著差异［(11.73±6.87) (nmol/mg)、(11.13±5.49) (nmol/mg)、(21.54±10.50) (nmol/mg)，0.05］，以高剂量组(50 mg/kg)更为显著［(9.96±4.08) (nmol/mg)，0.01］；③免疫组化显示PC组可以下调NF-κB p65蛋白的阳性表达率，与模型组比较有显著性差异（0.01)。结论 ①PC可减少脑缺血后自由基的生成，且以高剂量组的保护作用更加明显；②PC对局灶缺血性脑损伤保护作用的机制可能与抑制NF-кB活性，从而减少细胞凋亡有关。 【关键词】 原花青素 超氧化物歧化酶 丙二醛 核因子 　　Abstract: Objective To study the neuroprotective effects and mechanism of Procyanidins in focal cerebral ischemia injury in rats. Methods Sixty rats were randomly and equally divided into the sham-operative group，model group, focal cerebral ischemia group and Procyanidins groups of 50 mg/kg,100 mg/kg and 200 mg/kg. Embolization thread was inserted into all the rats except those in the sham-operative group for the establishment of model of middle cerebral artery occlusion. 2 week and 1 hours before MCAO，the rats in PC-treatment groups were provided corresponding doses of Procyanidins. The activity of superoxide dismutase (SOD) and contents of malondialdehyde (MDA) were measured after 24 hours focal cerebral ischemia. By immunohistochemical SABC method under high power lens, the immunohistochemistry changes of NF-кB were observed. Results ①The PC groups(50mg/kg，100mg/kg and 200mg/kg)could respectively increase the activity of SOD, which were evidently differential with model group[ (50.55±5.87) (U/mg prot),(51.44±7.06) (U/mg prot),(55.32±6.39) (U/mg prot) and (39.28±5.67) (U/mg prot), 0.01]. ②The contents of MDA in PC groups were