组蛋白乙酰化调控对新生大鼠大脑皮层损伤的保护作用
发布时间：2019-03-27 10:41
【摘要】：目的 研究组蛋白乙酰化调控对新生大鼠缺氧缺血大脑皮层损伤的保护作用。方法 将90只3日龄新生大鼠分为假手术组、缺氧缺血模型组以及组蛋白去乙酰化酶抑制剂丁酸钠组。模型组及丁酸钠组大鼠腹腔注射LPS(0.05 mg/kg)2 h后行右侧颈总动脉结扎并置于低氧舱中(6.5%氧浓度)90 min;假手术组腹腔注射生理盐水后仅分离暴露右侧颈总动脉,但不予结扎和低氧处理;丁酸钠组在建模后立即腹腔注射丁酸钠(300 mg/kg),每天1次,共治疗7 d,假手术组及模型组注射等体积生理盐水。模型建立后第7天,采用Western blot方法检测各组大脑皮层组蛋白H3(HH3),乙酰化组蛋白H3(AH3),B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、活化型半胱天冬酶-3(CC3),以及脑源性神经营养因子(BDNF)蛋白表达;采用免疫荧光法检测皮层细胞增殖指标Brd U表达。结果 丁酸钠组HH3/AH3比值显著低于模型组(P0.05),提示丁酸钠组HH3乙酰化程度增加;丁酸钠组凋亡相关蛋白Bcl-2/Bax比值较模型组显著增高(P0.05),CC3表达显著减少(P0.05),BDNF表达显著增加(P0.05);丁酸钠组较模型组皮层Brd U阳性细胞数显著增加(P0.05),主要表达在神经元。结论 组蛋白乙酰化水平增加可通过减少细胞凋亡及促进神经元再生保护新生大鼠大脑皮层损伤,其机制可能与BDNF表达增加相关。
[Abstract]:Objective to study the protective effects of protein acetylation on cerebral cortex injury in neonatal rats with hypoxic ischemia. Methods 90 3-day-old newborn rats were divided into three groups: sham-operation group, hypoxic-ischemic model group and sodium butyrate group, a histone deacetylase inhibitor. Rats in the model group and sodium butyrate group were injected intraperitoneally with LPS (0.05 mg/kg) for 2 hours after ligation of the right common carotid artery and placed in hypoxia chamber (6.5% oxygen concentration) 90 min;. In the sham operation group, the right common carotid artery was isolated and exposed only after intraperitoneal injection of normal saline, but no ligation or hypoxia was observed. Sodium butyrate group was injected intraperitoneally with sodium butyrate (300 mg/kg) once a day for 7 days. The rats in sham operation group and model group were injected with normal saline. On the 7th day after the establishment of the model, H3 (HH3), Bcl-2 (AH3), B cell lymphoma-2), (Bax), (Bcl-2-associated X protein) were detected by Western blot method in cerebral cortex of each group. Activated caspase-3 (CC3) and brain-derived neurotrophic factor (BDNF) protein expression; The expression of Brd U was detected by immunofluorescence assay. Results the ratio of HH3/AH3 in sodium butyrate group was significantly lower than that in model group (P0.05), suggesting that the acetylation degree of HH3 in sodium butyrate group was increased. The ratio of apoptosis-related protein Bcl-2/Bax in sodium butyrate group was significantly higher than that in model group (P0.05), while the expression of CC3 was significantly decreased (P0.05), BDNF expression increased (P0.05). The number of Brd U positive cells in cortex of sodium butyrate group was significantly higher than that of model group (P0.05), which was mainly expressed in neurons. Conclusion the increased histone acetylation level may protect the cerebral cortex injury by reducing apoptosis and promoting neuron regeneration in neonatal rats, which may be related to the increased expression of BDNF.
【作者单位】： 四川大学华西第二医院儿科/出生缺陷与相关妇儿疾病教育部重点实验室;
[Abstract]:Objective to study the protective effects of protein acetylation on cerebral cortex injury in neonatal rats with hypoxic ischemia. Methods 90 3-day-old newborn rats were divided into three groups: sham-operation group, hypoxic-ischemic model group and sodium butyrate group, a histone deacetylase inhibitor. Rats in the model group and sodium butyrate group were injected intraperitoneally with LPS (0.05 mg/kg) for 2 hours after ligation of the right common carotid artery and placed in hypoxia chamber (6.5% oxygen concentration) 90 min;. In the sham operation group, the right common carotid artery was isolated and exposed only after intraperitoneal injection of normal saline, but no ligation or hypoxia was observed. Sodium butyrate group was injected intraperitoneally with sodium butyrate (300 mg/kg) once a day for 7 days. The rats in sham operation group and model group were injected with normal saline. On the 7th day after the establishment of the model, H3 (HH3), Bcl-2 (AH3), B cell lymphoma-2), (Bax), (Bcl-2-associated X protein) were detected by Western blot method in cerebral cortex of each group. Activated caspase-3 (CC3) and brain-derived neurotrophic factor (BDNF) protein expression; The expression of Brd U was detected by immunofluorescence assay. Results the ratio of HH3/AH3 in sodium butyrate group was significantly lower than that in model group (P0.05), suggesting that the acetylation degree of HH3 in sodium butyrate group was increased. The ratio of apoptosis-related protein Bcl-2/Bax in sodium butyrate group was significantly higher than that in model group (P0.05), while the expression of CC3 was significantly decreased (P0.05), BDNF expression increased (P0.05). The number of Brd U positive cells in cortex of sodium butyrate group was significantly higher than that of model group (P0.05), which was mainly expressed in neurons. Conclusion the increased histone acetylation level may protect the cerebral cortex injury by reducing apoptosis and promoting neuron regeneration in neonatal rats, which may be related to the increased expression of BDNF.
【作者单位】： 四川大学华西第二医院儿科/出生缺陷与相关妇儿疾病教育部重点实验室;
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