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目的探讨缺氧缺血(HI)后神经型一氧化氮合酶(nNOS)的变化及神经生长因子(NGF)对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用。方法夹闭妊娠足月Wistar大鼠子宫血管,制成HIBD新生鼠模型。治疗组给予腹腔注射NGF4000U/kg,1次/d,分别用1、3、7次。在生后不同时间检测nNOS表达、NO含量及细胞凋亡数量。结果治疗组的NO含量明显降低,24h的NO含量(μmol/L)为23.98±2.37,72h为22.17±1.74,而HIBD组24h和72h的含量分别为31.64±3.23和30.31±1.76,两组比较,差异有统计学意义(P<0.05);治疗组nNOS的表达也下降,24h和72h的表达量(个/mm2)为26.8±0.8和29.2±1.8,而同时间点HIBD组nNOS表达量为54.7±2.2和34.5±1.4,两组比较,差异有统计学意义(P<0.05);神经细胞凋亡情况,治疗组72h、7d皮质和海马区的凋亡细胞数(个/mm2),分别为41.4±1.3、5.6±0.6和43.9±1.8、5.8±1.2,而HIBD组72h、7d皮质和海马区的凋亡细胞数分别为51.6±2.5、12.6±1.4和58.7±2.6、15.2±1.7,治疗组的凋亡细胞数明显降低,同时期同部位比较均有统计学意义(P<0.05)。结论本研究证实NGF对新生大鼠HIBD有保护作用,通过抑制nNOS的表达,降低了炎性细胞因子NO的含量,减轻了HIBD后的脑细胞凋亡,证实NGF抗凋亡作用与抑制nNOS的表达从而减少NO生成有关。
Objective To investigate the changes of neuronal nitric oxide synthase (nNOS) after hypoxia-ischemia (HI) and the protective effect of nerve growth factor (NGF) on hypoxic-ischemic brain damage (HIBD) in neonatal rats. Methods The uterine vessels of pregnant Wistar rats were occluded and made into newborn HIBD model. The treatment group was given intraperitoneal injection of NGF 4000U / kg, 1 / d, respectively, 1,3,7 times. At different times after birth, nNOS expression, NO content and the number of apoptotic cells were detected. Results The content of NO in the treatment group was significantly lower than that in the control group. The content of NO at 24 h (μmol / L) was 23.98 ± 2.37 and at 22 h was 22.17 ± 1.74, while in HIBD group at 24 h and 72 h were 31.64 ± 3.23 and 30.31 ± 1.76 respectively , The difference was statistically significant (P <0.05). The expression of nNOS also decreased in the treatment group, and the expression levels in 24 h and 72 h (a / mm2) were 26.8 ± 0.8 and 29.2 ± 1.8, while the expression of nNOS in HIBD group was 54.7 ± 2.2 and 34.5 ± 1.4, respectively. There was significant difference between the two groups (P <0.05); The apoptosis of neurons, the number of apoptotic cells in cortex and hippocampus at 72h, 7d Were 41.4 ± 1.3,5.6 ± 0.6 and 43.9 ± 1.8,5.8 ± 1.2, respectively. The number of apoptotic cells in cortex and hippocampus in HIBD group at 72h and 7d were 51.6 ± 2.5, 12.6 ± 1.4 and 58.7 ± 2.6, 15.2 ± 1.7 respectively, The number of apoptotic cells in the treatment group was significantly lower than that in the same period (P <0.05). Conclusions This study demonstrates that NGF can protect HIBD in neonatal rats, and can inhibit the expression of nNOS, reduce the content of inflammatory cytokines NO and reduce the apoptosis of brain cells after HIBD. It is concluded that the anti-apoptotic effects of NGF and the inhibition of nNOS Expression thus reducing NO production.