STUDY OF CEREBRAL ISCHEMIC TOLERANCE USING MAGNETIC RESONANCE AND IMMUNOHISTOCHEMICAL TECHNIQUES : PART 1

使用磁共振和免疫组织化学技术研究脑缺血耐受：第 1 部分

• 批准号: 05670584
• 负责人: NARITOMI Hiroaki
• 金额: $ 1.41万
• 依托单位: NATIONAL CARDIOVASCULAR CENTER RESEARCH INSTITUTE
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05670584/
• 关键词: cerebral ischemia; heat-shock protein; ischemic tolerance; astrocyte; energymetabolism; 31P-NMR spectroscopy; hyppocampus; delayd neuronal death; エネルギー代謝; ^<31>P NMRスペクトロスコピー; 遅発性神経細胞壊死

In order to clarify wehther focal ischemic insults can cause ischemic tolerance in neurons in the surrounding areas, immunohistochemical and 31p-NMR spectroscopic studes were undertaken in mongolian gerbils. Right cortical infarction was induced by skull magnet-minute magnetite particle intravenous injection methods or middle cerebral artery occlusion. The infarction was found to cause no induction of HSP70 mRNA in infarcted areas and the adjacent hippocampus. Immunohistochemical studies showed GFAP-positive astrocytes accumulation in the infarcted area and the adjacent hippocampal CA1 sectros at 3 and 7 days after infarction. 5-min forebrain ischemia conducted at 1,3 or 7 days after infarction caused diffuse neuronal death in the non-infarcted side CA1 sectors. However, 5 min forebrain ischemia at 3 days after infarction brought about small number of neuronal death in the infarcted side CA1 sector. This ischemic tolerance was most remarkable in the CA1 sector adjacent the infarction. Less prominent ischemic tolerance was observed in a group with 5-min ischemia at 1 day after infarction. Yet, no such tolerance was observed in agroup with 5 min ischemia at 7 days after infarction. 31P-NMR studies indicated that forebrain ischemia caused severe energy disturbance irrespectively of existence of infarction. The results suggest that during several days after focal infarction, neurons in the surrounding areas may show ischemic tolerance. This tolerance is not attributable to induction of heat-shock protein or improvement of energy failure. Presumably, reactive atrocytes may exert protective effects on the adjacent neurons.

为阐明局灶性脑缺血是否能引起周围神经元的缺血耐受，本文对沙土鼠进行了免疫组织化学和~（31）P-NMR波谱研究。采用颅磁-微磁颗粒静脉注射法或大脑中动脉闭塞法诱发右侧皮质梗死。脑梗死后梗死区及邻近海马HSP 70 mRNA无明显表达。免疫组化结果显示，GFAP阳性星形胶质细胞聚集在梗死区和邻近的海马CA 1 sectros在梗死后3和7天。5-脑梗死后1、3或7天进行的min前脑缺血导致非梗死侧CA 1区弥漫性神经元死亡。然而，5分钟前脑缺血在梗死后3天带来了少量的神经元死亡，在梗死侧CA 1区。这种缺血耐受在邻近梗死的CA 1区最为显著。在梗死后1天缺血5分钟的组中观察到不太突出的缺血耐受性。而缺血5 min组在7 d时则无这种耐受。~（31）P-NMR研究表明，前脑缺血引起严重的能量紊乱，与是否存在梗塞无关。结果表明，在局灶性脑梗死后的几天内，周围区域的神经元可能表现出缺血耐受性。这种耐受性不是由于热休克蛋白的诱导或能量衰竭的改善。推测反应性萎缩细胞可能对邻近神经元发挥保护作用。

项目成果

Miyashita K,Abe H,Nakajima T.Naritomi H: "Induction of ischemic tolerance in gubil hyppocampus by pretreatment with focal ischemia." Neuro Report. 6. 46-48 (1994)

Miyashita K、Abe H、Nakajima T.Naritomi H：“通过局灶性缺血预处理诱导 gubil 海马的缺血耐受性。”

Suzuki M,Naritomi H,Sasaki M,Miyashita K,Kadota E,Sawada T: "Protection of unilateral CA1 neurons from delayd neuronal death due to the preceding adjacent cortical infarction." J Cereb Blood Flow Metab. 13. S765 (1993)

Suzuki M、Naritomi H、Sasaki M、Miyashita K、Kadota E、Sawada T：“保护单侧 CA1 神经元免受因先前相邻皮质梗塞导致的延迟性神经元死亡。”

Suzuki M,Naritomi H,Sasaki M,Miyashita K,Kadota E.Sawada T: "Protection of unilateral CAI neurons from delayed neuronal cleath clcee to the precedeiy adjacent cortical infarction." J Cereb Blood Flow Metab. 13. S765 (1993)

Suzuki M、Naritomi H、Sasaki M、Miyashita K、Kadota E.Sawada T：“保护单侧 CAI 神经元免受延迟神经元裂隙到先前相邻皮质梗塞的影响。”

Miyashita K,Abe E,Nakajima T,Ishikawa A,Nishiura M,Sawada T,Naritomi H: "Induction of ischemic tolerance in gerbil hyppocampus by pretreatment with focal ischemia." Neuro Report. 6. 464-48 (1994)

Miyashita K、Abe E、Nakajima T、Ishikawa A、Nishiura M、Sawada T、Naritomi H：“通过局部缺血预处理诱导沙鼠海马的缺血耐受性。”

Suzuki M,Naritomi H,Sasaki M.Miyashita K,Kadota E,Sawada T: "Protection of unilstcral CA1 neurons from delayed neuronel death due to the precealing adjaccut cortical infarction." J Cereb Blood Flow Metab. 13. s765- (1993)

Suzuki M、Naritomi H、Sasaki M.Miyashita K、Kadota E、Sawada T：“保护单 CA1 神经元免受因预封闭皮质梗塞导致的延迟性神经元死亡。”