The Induction of the Heat Shock Protein under the Hypoxic Condition

缺氧条件下热激蛋白的诱导

• 批准号: 03670721
• 负责人: ITO Yusuke
• 金额: $ 1.47万
• 依托单位: Toyama Medical and Pharmaceutical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1992
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670721/
• 关键词: HYPOXIA; HEAT SHOCK PROTEIN; 熱ショック蛋白質

It is known that heat shock protein (HSP) is induced responding to various stresses not only a heat shock which is the origin of a name of this protein. One of inducible stresses is the ischemic condition. In this study we investigate the locality of HSP induction under the low oxygen condition using a hypoxic model of 5 % oxygen inhalation that we have used since before in this research and 2 min anoxia model suspending the ventilator. Additionally, we persuaded the fluctuation of HSP induction quantitatively by the method of immunoblotting technique. In the ischemic model of gerbil the HSP was induced strongly in our experiment as well as previously reported. On the other hand, the induction of HSP was slight in the rat hypoxic model and even in the rat ischemic model. Two reasons are conceivable to this result. There are some reports since before that rat is a comparatively strong animal species in the low oxygen condition. Therefore,HSP induction was small in hypoxic rat's brain. A … More nother reason is that our experiment model of low oxygen condition accompanies a decrease of the heart rate unlike a brain ischemic model. Therefore an influence is exerted on a whole body. The incomplete ischemic condition like this becomes a fatal blow for a digestive organ system particularly the small intestine. Acker et al reported that in the case of a decreased blood flow a blood flow circulates to a brain and a heart preferentially. Therefore,these organs were protected in the incomplete ischemia. When an extent of a hypoxic load is strong,the induction of HSP increased. It peaked in a day or two. The phenomenon of ischemic tolerance well known if it gets weak ischemia done before severe ischemia is suffered. We tried to apply the 2nd load in a day after a mild hypoxic event. Surely the HSP was induced, but the injury was accumulative rather than the acquisition of tolerance. Although congestion and bleeding were seen at the small intestine and the cecum,there was not a change especially in a nerve cell of the nerve terminals which distributes to intestines even in such a case. The acquisition of ischemic tolerance by the HSP may limit to a nerve cell only. Less

已知热休克蛋白（HSP）不仅是热休克蛋白（HSP）的名称来源，还可被诱导对各种应激反应。诱导应激之一是缺血状态。本研究采用本研究中一直使用的5%氧吸入缺氧模型和2min呼吸机暂停缺氧模型，研究了低氧条件下HSP诱导的部位。此外，我们还用免疫印迹技术定量地研究了HSP诱导的波动性。在沙土鼠的缺血模型中，HSP在我们的实验中被强烈地诱导，正如以前报道的那样。另一方面，在大鼠缺氧模型中，甚至在大鼠缺血模型中，HSP的诱导轻微。造成这一结果的原因有两个。此前有报道称大鼠是低氧条件下较强的动物物种。因此，缺氧大鼠脑内HSP的诱导作用较小。一 ...更多信息 另一个原因是我们的低氧条件的实验模型伴随着心率的降低，这与脑缺血模型不同。因此，一种影响作用于整个身体。像这样的不完全缺血状态对消化器官系统特别是小肠来说是致命的打击。阿克等人报道，在血流减少的情况下，血流优先循环到大脑和心脏。因此，这些器官在不完全缺血中受到保护。当低氧负荷程度较强时，HSP的诱导增加。一两天内达到顶峰。缺血耐受现象是指在严重缺血之前先进行弱缺血。我们尝试在轻度缺氧事件后的一天内应用第二次负荷。HSP确实是诱发的，但损伤是累积性的，而不是耐受性的获得。虽然在小肠和盲肠处观察到充血和出血，但即使在这种情况下，也没有变化，特别是在分布到肠的神经末梢的神经细胞中。HSP获得缺血耐受可能仅限于神经细胞。少

项目成果

Yamazaki M.,Ito Y.,Kuze S.,Shibuya N.,and Mmose Y.:"Effects of ketamine on voltage-dependent Ca^<2+> currents in single smooth muscle cells from rabbit portal vein." Pharmacol.45. 162-169 (1992)

Yamazaki M.、Ito Y.、Kuze S.、Shibuya N. 和 Mmose Y.：“氯胺酮对兔门静脉单个平滑肌细胞中电压依赖性 Ca^2 > 电流的影响。”

M.Yamazaki T.Masuda S.Kuze Y.Ito: "Changes in the Rat Striatum Catecholamine during Hypoxic Hypoxia with Reference to Protective Effect of Flunarizine" Pharmacology and Toxicology.

M.Yamazaki T.Masuda S.Kuze Y.Ito：“缺氧时大鼠纹状体儿茶酚胺的变化与氟桂利嗪的保护作用有关”药理学和毒理学。

KUZE S,NARUSE T,YAMAZAKI M,HIROTA K,ITO Y,and MIYAHARA T: "Effects of sodium L-Lactate and sodium racemic lactate on intraoperative acid-base status." Anesth.Analg.75. 702 707 (1992)

KUZE S、NARUSE T、YAMAZAKI M、HIROTA K、ITO Y 和 MIYAHARA T：“L-乳酸钠和消旋乳酸钠对术中酸碱状态的影响。”

Yamazaki M., Ito Y., Kuze S., Shibuya N., and Momose Y.: "Effects of ketamine on voltage-dependent Ca2+ currents in single smooth muscle cells from rabbit portal vein." Pharmacol.45. 162-169 (1992)

Yamazaki M.、Ito Y.、Kuze S.、Shibuya N. 和 Momose Y.：“氯胺酮对兔门静脉单个平滑肌细胞中电压依赖性 Ca2+ 电流的影响。”

YAMAZAKI M,ITO Y,KUZE S,SHIBUYA N,and MOMOSE Y: "Effects of ketamine on voltage-dependent Ca2+ currents in single smooth muscle from rabbit portal vein." Pharmacol.45. 162 169 (1992)

YAMAZAKI M、ITO Y、KUZE S、SHIBUYA N 和 MOMOSE Y：“氯胺酮对兔门静脉单个平滑肌中电压依赖性 Ca2+ 电流的影响”。