Expression of Mn-SOD gene in the neonatal rat with hypoxic-ischemic brain damage.

Mn-SOD基因在缺氧缺血性脑损伤新生大鼠中的表达

• 批准号: 06671168
• 负责人: TAKADA Satoshi
• 金额: $ 1.34万
• 依托单位: Kobe University. School of Medicine, Department of Pediatrics
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06671168/
• 关键词: Mn-Superoxide dismutase; Hypoxic-ischemic encephalopathy; Dexamethasone; Immuno-peroxidase staining; Northern Blotting; Mn-Superoxide desmutase; Mn-SOD

1. Expression of Mn-SOD gene in the developing rat brain.Expression of Mn-SOD mRNA was studied in the developing rat brain by using Northern blotting analysis. Mn-SOD mRNA was observed in the fetal rat brain on gestational day 18, and its level increased during early neonatal days. Immuno-histochemical staining revealed that Mn-SOD positive cells were rich in CA3 area in the hippocampus in these days.2. Effect of hypoxic-ischemic brain damage on the expression of Mn-SOD.Ischemic changes were most evident in the cortex, hippocampus, striatum and thalamus. The infiltration of Mn-SOD positive astrocytes was observed in the regions surrounding these involved areas.3. Effect of dexamethasone on the expression of Mn-SOD.The treatment with dexamethasone suppressed the expression of Mn-SOD in the developing rat brain. In the rats treated with dexamethasone, both the number of GFAP positive cells and the number of the cortical cells in the cerebral cortex were less than those in the control rats. The administration of the dexamethasone also weakened the intensity of MBP immunostaining. Pretreatment with dexamethasone protected the developing brain from hypoxic-ischemic injury, and the infiltration of Mn-SOD positive astrocytes decreased in our experiment. These results suggest that the protection by dexamethasone was due to the suppression of the glial and neuronal cell maturation.

1.用北方印迹法研究了Mn-SOD基因在大鼠脑发育过程中的表达。Mn-SOD mRNA在孕18天的胎鼠脑内表达，在新生儿早期表达增加。免疫组化染色显示，Mn-SOD阳性细胞在海马CA 3区较丰富.缺氧缺血性脑损伤对Mn-SOD表达的影响。缺血性改变以皮层、海马、纹状体和丘脑最为明显。Mn-SOD阳性星形胶质细胞浸润于病变周围.地塞米松对Mn-SOD表达的影响地塞米松可抑制发育期大鼠脑组织Mn-SOD的表达。地塞米松组大鼠大脑皮质GFAP阳性细胞数和皮质细胞数均低于对照组。地塞米松的施用也减弱了MBP免疫染色的强度。地塞米松预处理可明显减轻缺氧缺血性脑损伤，减少Mn-SOD阳性星形胶质细胞的浸润。这些结果表明，地塞米松的保护作用是由于抑制神经胶质细胞和神经元细胞的成熟。

项目成果

高田哲: "新生児仮死(低酸素性虚血性脳症)" 小児内科. 27. 681-687 (1995)

Satoshi Takada：“新生儿窒息（缺氧缺血性脑病）”小儿内科 27. 681-687 (1995)。

Yamei Liu.: "Preventive effects of dexamethasone on hypoxic-ischemic brain damage in the neonatal rat." Brain and Development.17. 186-192 (1995)

刘亚梅：“地塞米松对新生大鼠缺氧缺血性脑损伤的预防作用。”

Noriaki Ohnishi.: "Development and evaluation of propentofylline suppositories : in vitro release,stability and rectal absorption characteristics of suppositories." The Japanese Journal of TDM.12. 409-415 (1994)

Noriaki Ohnishi.：“丙戊茶碱栓剂的开发和评估：栓剂的体外释放、稳定性和直肠吸收特性。”

Naoki Yokoyama.: "Effects of maternal administration of dexamethasone and thyrotropin-releasing hormone on fetal pulmonary surfactant synthesis." Biology of the Neonate.68. 39-46 (1995)

Naoki Yokoyama：“母亲服用地塞米松和促甲状腺素释放激素对胎儿肺表面活性物质合成的影响。”

Satoshi Takada, Hajime Nakamura.: "Neonatal Asphyxia (Hypoxic-Ischemic Encephalopathy.)" Japanese Journal of Pediatric Medicine.27. 39-46 (1995)

Satoshi Takada、Hajime Nakamura.：“新生儿窒息（缺氧缺血性脑病）。”日本儿科医学杂志.27。