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; 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

众所周知，热休克蛋白（HSP）被诱导到各种应力上，不仅是热休克，这是该蛋白质名称的起源。诱导的应力之一是缺血状况。在这项研究中，我们使用以前在这项研究以来使用的5％氧气吸入的低氧模型和悬挂呼吸机的2分钟缺氧模型，研究了低氧条件下HSP诱导的位置。此外，我们通过免疫印迹技术的方法说服了HSP诱导的波动。在沙鼠的缺血模型中，HSP在我们的实验中强烈诱导，并以前报道。另一方面，在大鼠低氧模型甚至大鼠缺血模型中，HSP的诱导略有略有诱导。这个结果可以想象两个原因。有一些报道，因为在低氧气状态下，大鼠是一种相对强的动物物种。因此，在低氧大鼠的大脑中，HSP诱导很小。一个…没有理由的是，我们低氧条件的实验模型涉及与脑缺血模型不同的心率降低。因此，影响对整个身体施加。对于消化器官系统，尤其是小肠，不完全的缺血状况成为致命的打击。 Acker等人报道说，在减少血流的情况下，A血流循环到大脑和心脏。因此，器官在不完全缺血中受到保护。当低氧负载的程度强大时，HSP的诱导增加。它在一两天内达到顶峰。缺血性耐受性的现象是否在严重缺血之前弱缺血。在轻度低氧事件发生后的第二天，我们尝试在第二次载荷。当然，HSP是被诱导的，但是损伤是累积的，而不是在小肠和盲肠上看到拥塞和出血，尤其是在神经末端的神经细胞中，即使在这种情况下也分布在肠道上。 HSP对缺血性耐受性的获取可能仅限于神经细胞。较少的