摘要目的:观察白杨素对缺血缺氧性脑病模型新生大鼠的脑保护作用，探讨其作用机制。方法:将大鼠按随机数字表法分为假手术组、模型组和白杨素低、高剂量组，每组12只。除假手术组外，其余各组大鼠制备缺血缺氧性脑病大鼠模型。模型制作完成后，白杨素低、高剂量组立刻腹腔注射白杨素30、60 mg/kg，假手术组和模型组腹腔注射等体积生理盐水，1次/d，连续给药4 d。采用HE染色观察各组大鼠脑组织病理学改变，生化测定脑组织SOD、CAT、MDA水平，采用Western blot法检测脑组织血红素加氧酶-1(heme oxygenase-1, HO-1)、转录因子NF-E2相关因子2(NF-E2-related factor 2, Nrf2)蛋白表达。结果:假手术组大鼠神经细胞排列规则有序，胞核圆形，核仁明显；模型组大鼠脑组织水肿，神经细胞排列松散；白杨素低、高剂量组神经细胞变性、坏死较模型组减轻。与模型组比较，白杨素低、高剂量组大鼠脑组织中SOD[(55.74±5.14)U/mg、(69.84±5.05)U/mg比(37.64±6.41)U/mg]、CAT[(2.44±0.22)U/mg、(2.59±0.42)U/mg比(2.08±0.37)U/mg]活性升高( P<0.05)，MDA[(3.74±0.05)mmol/mg、(2.60±0.18)mmol/mg比(4.35±0.24)mmol/mg]水平降低( P<0.05)；脑组织HO-1[(0.43±0.08)、(1.02±0.15)比(0.14±0.07)]、Nrf2[(0.48±0.07)、(0.79±0.09)比(0.26±0.08)]蛋白表达增加( P<0.05)。 结论:白杨素可减轻缺血缺氧性脑病大鼠神经损伤，其机制可能与上调HO-1、Nrf2蛋白表达有关。

abstractsObjective:To investigate the protective effect of chrysin on the newborn rats with ischemic hypoxic brain damage and its related mechanism.Methods:The rats were randomly divided into sham-operated group, model group, low and high-dosage group of chrysin with 12 rats in each group. Except sham-operated group, the rats in other three groups were used as hypoxic-ischemic encephalopathy model. After the modeling, the rats in the low and high dosage groups were intraperitoneally injected with 30 mg/kg and 60 mg/kg chrysinimmediately, while the rats in the sham-operated group and the model group were intraperitoneally injected with equal volume of normal saline for 4 days. The HE staining was used to observe the protective effect of drugs on brain. The superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) levels in cells were measured by biochemical method. Western blot was used to detect the expression of heme oxygenase-1 (HO-1) and transcription factor NF-E2-related factor 2 (Nrf2).Results:The neurons in the cortex of rats in sham-operated group were arranged orderly with round nuclei and obvious nucleoli; the brain tissue of rats in model group showed edema and the arrangement of neurons was loose, the degeneration and necrosis of neurons in low and high dosage of chrysin groups were less than those in model group. Compared to the model group, the SOD activity (55.74 ± 5.14 U/mg, 69.84 ± 5.05 U/mg vs. 37.64 ± 6.41 U/mg) and CAT activity (2.44 ± 0.22 U/mg, 2.59 ± 0.42 U/mg vs. 2.08 ± 0.37 U/mg) in the brain tissue of rats in the low and high dose group were significantly increased ( P<0.05). The MDA level (3.74 ± 0.05 mmol/mg, 2.60 ± 0.18 mmol/mg vs. 4.35 ± 0.24 mmol/mg) in rat brain tissue of low and high dose group was significantly decreased ( P<0.05). The expressions of HO-1 (0.43 ± 0.08, 1.02 ± 0.15 vs. 0.14 ± 0.07) and Nrf2 (0.48 ± 0.07, 0.79 ± 0.09 vs. 0.26 ± 0.08) protein in rat brain tissue of low and high dose group were significantly decreased ( P<0.05). Conclusions:The chrysin could alleviate nerve injury in rats with hypoxic-ischemic encephalopathy, and its mechanism may be related to the up-regulated HO-1 and Nrf2 protein expression.