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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Yamashita K, Kataoka Y, Yamashita Y S, Himeno A, Tsutsumi K, Niwa M, Taniyama K

Department of Pharmacology, Nagasaki University School of Medicine, Japan.

Clin Exp Pharmacol Physiol Suppl. 1995 Dec;22(1):S277-8. doi: 10.1111/j.1440-1681.1995.tb02915.x.

When delayed neuronal death occurred in the hippocampus CA1 pyramidal cell layer of stroke-prone spontaneously hypertensive rats (SHRSP) at 4 and 7 days after a 10 min bilateral carotid occlusion and reperfusion, intense endothelin-1 (ET-1)- and ET-3-like immunoreactivities became evident in astrocytes in the damaged hippocampus CA1 subfields. 2. We also observed that microglia equipped with an ETB receptor aggregated within the CA1 pyramidal cell layer with neuronal death. 3. There was a dramatic increase in nitric oxide synthase (NOS) activity in astrocytes and microglia in the damaged hippocampus CA1 subfields. 4. Thus, the possibility that microglia with the ETB receptor are activated to produce NO, a neurotoxic factor, by astrocytic ET-1 and ET-3 produced in response to transient forebrain ischaemia would have to be considered.

在双侧颈动脉闭塞10分钟并再灌注后的第4天和第7天，易卒中型自发性高血压大鼠（SHRSP）海马CA1锥体细胞层出现延迟性神经元死亡时，受损海马CA1亚区的星形胶质细胞中出现强烈的内皮素-1（ET-1）和内皮素-3样免疫反应性。2. 我们还观察到，配备ETB受体的小胶质细胞在CA1锥体细胞层内随着神经元死亡而聚集。3. 受损海马CA1亚区的星形胶质细胞和小胶质细胞中的一氧化氮合酶（NOS）活性显著增加。4. 因此，必须考虑这样一种可能性，即配备ETB受体的小胶质细胞被星形胶质细胞产生的ET-1和ET-3激活，以产生作为神经毒性因子的一氧化氮，这是对短暂性前脑缺血的反应。

Yamashita K, Kataoka Y, Yamashita Y S, Himeno A, Tsutsumi K, Niwa M, Taniyama K

Department of Pharmacology, Nagasaki University School of Medicine, Japan.

Clin Exp Pharmacol Physiol Suppl. 1995 Dec;22(1):S277-8. doi: 10.1111/j.1440-1681.1995.tb02915.x.

When delayed neuronal death occurred in the hippocampus CA1 pyramidal cell layer of stroke-prone spontaneously hypertensive rats (SHRSP) at 4 and 7 days after a 10 min bilateral carotid occlusion and reperfusion, intense endothelin-1 (ET-1)- and ET-3-like immunoreactivities became evident in astrocytes in the damaged hippocampus CA1 subfields. 2. We also observed that microglia equipped with an ETB receptor aggregated within the CA1 pyramidal cell layer with neuronal death. 3. There was a dramatic increase in nitric oxide synthase (NOS) activity in astrocytes and microglia in the damaged hippocampus CA1 subfields. 4. Thus, the possibility that microglia with the ETB receptor are activated to produce NO, a neurotoxic factor, by astrocytic ET-1 and ET-3 produced in response to transient forebrain ischaemia would have to be considered.

在双侧颈动脉闭塞10分钟并再灌注后的第4天和第7天，易卒中型自发性高血压大鼠（SHRSP）海马CA1锥体细胞层出现延迟性神经元死亡时，受损海马CA1亚区的星形胶质细胞中出现强烈的内皮素-1（ET-1）和内皮素-3样免疫反应性。2. 我们还观察到，配备ETB受体的小胶质细胞在CA1锥体细胞层内随着神经元死亡而聚集。3. 受损海马CA1亚区的星形胶质细胞和小胶质细胞中的一氧化氮合酶（NOS）活性显著增加。4. 因此，必须考虑这样一种可能性，即配备ETB受体的小胶质细胞被星形胶质细胞产生的ET-1和ET-3激活，以产生作为神经毒性因子的一氧化氮，这是对短暂性前脑缺血的反应。