【摘要】：目的 研究組蛋白乙�；{(diào)控對新生大鼠缺氧缺血大腦皮層損傷的保護作用。方法 將90只3日齡新生大鼠分為假手術(shù)組、缺氧缺血模型組以及組蛋白去乙酰化酶抑制劑丁酸鈉組。模型組及丁酸鈉組大鼠腹腔注射LPS(0.05 mg/kg)2 h后行右側(cè)頸總動脈結(jié)扎并置于低氧艙中(6.5%氧濃度)90 min;假手術(shù)組腹腔注射生理鹽水后僅分離暴露右側(cè)頸總動脈,但不予結(jié)扎和低氧處理;丁酸鈉組在建模后立即腹腔注射丁酸鈉(300 mg/kg),每天1次,共治療7 d,假手術(shù)組及模型組注射等體積生理鹽水。模型建立后第7天,采用Western blot方法檢測各組大腦皮層組蛋白H3(HH3),乙�；M蛋白H3(AH3),B細(xì)胞淋巴瘤-2(Bcl-2)、Bcl-2相關(guān)X蛋白(Bax)、活化型半胱天冬酶-3(CC3),以及腦源性神經(jīng)營養(yǎng)因子(BDNF)蛋白表達;采用免疫熒光法檢測皮層細(xì)胞增殖指標(biāo)Brd U表達。結(jié)果 丁酸鈉組HH3/AH3比值顯著低于模型組(P0.05),提示丁酸鈉組HH3乙�；潭仍黾�;丁酸鈉組凋亡相關(guān)蛋白Bcl-2/Bax比值較模型組顯著增高(P0.05),CC3表達顯著減少(P0.05),BDNF表達顯著增加(P0.05);丁酸鈉組較模型組皮層Brd U陽性細(xì)胞數(shù)顯著增加(P0.05),主要表達在神經(jīng)元。結(jié)論 組蛋白乙�；皆黾涌赏ㄟ^減少細(xì)胞凋亡及促進神經(jīng)元再生保護新生大鼠大腦皮層損傷,其機制可能與BDNF表達增加相關(guān)。
[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.
【作者單位】： 四川大學(xué)華西第二醫(yī)院兒科/出生缺陷與相關(guān)婦兒疾病教育部重點實驗室;

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