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目的研究去铁胺(DFO)对新生鼠缺氧缺血性脑损伤(HIBD)后海马CA1区5-溴脱氧尿嘧啶(Brd U)和胶原纤维酸性蛋白(GFAP)表达变化的影响。方法通过结扎并剪断7日龄新生Wistar大鼠右侧颈总动脉,吸入8%O_2+92%N_21 h制备新生鼠HIBD模型。随机将HIBD鼠分为模型组和实验组,同时设置假手术组;实验组于脑缺氧缺血后立即腹腔注射DFO 0.2 mg·g~(-1)·d~(-1),然后分别于24,48 h各注射1次;模型组于相同时间点给予同体积0.9%Na Cl腹腔注射;假手术组不注射。以间接免疫荧光组织化学方法检测各组大鼠给药后第4天海马CA1区Brd U阳性细胞数和GFAP表达变化,光镜下观察脑组织病理改变。结果 3组新生Wistar大鼠脑组织病理改变:假手术组无异常病理改变;模型组海马CA1区细胞层次减少,排列紊乱,出现胶质细胞增生,大量神经细胞核固缩、碎裂;实验组大鼠脑病理改变较模型组减轻。3组新生鼠海马CA1区5-溴脱氧尿嘧啶(Brd U)阳性细胞数比较:给药后第4天,假手术组、模型组和实验组Brd U阳性细胞数分别为14.50±11.14、35.63±15.79和51.63±17.79,与假手术组比较,模型组差异有统计学意义(P<0.01);与模型组比较,实验组差异有统计学意义(P<0.05)。3组新生鼠海马CA1区胶原纤维酸性蛋白表达:给药后第4天,假手术组、模型组和实验组积分光密度值分别为0.16±0.46×10~(-2),0.20±0.65×10~(-2),0.28±0.74×10~(-2),与假手术组比较,模型组差异有统计学意义(P<0.001);与模型组比较,实验组差异有统计学意义(P<0.001)。结论 DFO可减轻新生Wistar大鼠HIBD后脑组织病理损害,促进海马CA1区Brd U、GFAP表达增加,提示DFO早期干预可促进新生Wistar大鼠HIBD后受损神经细胞的再生。
Objective To investigate the effect of deferoxamine (DFO) on the expression of BrdU and GFAP in hippocampal CA1 area of neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods The right common carotid artery in 7-day-old Wistar rats was induced by ligating and shearing. HIBD model was established by inhalation of 8% O2 + 92% N-21 h. The HIBD mice were randomly divided into model group and experimental group, and sham-operated group was set at the same time. In the experimental group, intraperitoneal injection of DFO 0.2 mg · g ~ (-1) d ~ (-1) The rats in the model group were intraperitoneally injected with 0.9% Na Cl at the same time point, while those in the sham operation group were not injected. The number of BrdU positive cells and the expression of GFAP in hippocampal CA1 area were detected by indirect immunofluorescence histochemistry at 4 days after administration. The pathological changes of brain tissue were observed under light microscope. Results The histopathological changes in the brain tissue of 3 Wistar rats were as follows: There were no abnormal pathological changes in the sham operation group. The levels of hippocampus CA1 in the model group were reduced and arranged disorderly, with glial cell proliferation, a large number of nuclear pyknosis and fragmentation. Pathological changes in rat brain lessened compared with model group. BrdU positive cells in hippocampal CA1 area of neonatal rats in three groups were compared: On the fourth day after administration, the number of BrdU positive cells in sham operation group, model group and experimental group were respectively 14.50 ± 11.14 and 35.63 ± 15.79 and 51.63 ± 17.79 respectively. There was significant difference between the model group and the sham operation group (P <0.01). Compared with the model group, there was significant difference in the experimental group (P <0.05). At 4 days after administration, the integral optical density values of the sham operation group, model group and experimental group were 0.16 ± 0.46 × 10 -2 and 0.20 ± 0.65 × (P <0.001). Compared with the model group, the difference between the experimental group and the model group was statistically significant (P <0.001). Compared with the sham operation group, the difference was statistically significant P <0.001). Conclusion DFO can attenuate the pathological changes of brain tissue in neonatal Wistar rats after HIBD and increase the expression of Brd U and GFAP in hippocampal CA1 region. It suggests that early DFO can promote the regeneration of injured neurons in neonatal Wistar rats after HIBD.