The study for the mechanism of loss of hair after the transient ischemia

七十二 kd 热休克蛋白 (HSP72) 是细胞在应激（例如缺血的情况下）中诱导的应激标记物之一。最近的研究表明，HSP72 是一种“分子伴侣”，可以保护细胞免受各种应激，并且 HSP72 诱导的时间特征与缺血脆弱性相关。在本研究中，我们试图分析短暂性缺血不同时期后皮瓣浅层毛囊和深层毛囊角质形成细胞中HSP72诱导的时间分布，并探讨这些细胞之间缺血耐受性差异的原因。我们使用Wister大鼠腹部皮瓣，将其分为三组：假手术对照组（n = 27）、2小时缺血组（n = 25）和缺血2小时组（n = 27）。 8小时缺血组(n=25)。在再灌注后 8、24、48、96 小时和 7 天的时间段，我们检查了它们的组织学变化，并对 HSP72 和 caspas e-3 进行了免疫染色（每个时间点 n=5）。此外，我们还进行了TUNEL染色来检测细胞凋亡。结果，无论缺血应激如何，所有组的浅部毛囊中的角质形成细胞随着时间的推移都显示HSP72阳性，并且它们的TUNEL染色不呈阳性。深部毛囊中，假对照组细胞再灌注后未见免疫反应性，TUNEL染色未见阳性细胞。缺血2小时组，角质形成细胞对HSP72的反应性逐渐增强；因此，他们的 TUNEL 染色也根本没有阳性细胞。在8小时缺血组中，HSP72的反应性在再灌注后8小时显现，并在再灌注后24小时突然下降；结果显示 TUNEL 染色呈阳性。再灌注后8小时，它们还表达活性形式的caspase-3。我们得出结论，HSP72表达的这些差异与深部卵泡对缺血的脆弱性有关。 8小时的缺血仅在深层毛囊中引起HSP72诱导的紊乱，因此深层毛囊中的角质形成细胞出现凋亡。并且这种细胞凋亡伴随着caspase-3的激活。较少的

Seventy-two-kd heat-shock protein (HSP72) is one of the stress markers induced in cells under stress, such as in the case of ischemia. Recent studies have suggested that HSP72 is a "molecular chaperone" to protect cells from various kinds of stress, and that the temporal profile of HSP72 induction is related to ischemic vulnerability. In this study, we attempted to analyze the temporal profiles of HSP72 induction in keratinocytes in the shallow hair follicles and the deep hair follicles in skin flaps after various periods of transient ischemia, and we investigated the reason why there were differences in ischemic tolerance between these cells.We used the abdominal skin flap of Wister rats, which were divided into three groups: the sham control group (n=27), the 2-hour ischemia group (n=25), and the 8-hour ischemia group (n=25). At periods of 8, 24, 48, 96 hours, and 7 days after reperfusion, we examined them for any histological changes and performed immunostaining for HSP72 and caspas … More e-3 (n=5, each time point). In addition, we performed TUNEL stain for detecting apoptosis.As a result, the keratinocytes in the shallow hair follicles in all groups revealed positive for HSP72 through the time course, regardless of the ischemic stresses, and they were not positive for TUNEL stain. In the deep hair follicles, the cells in the sham control group revealed no immunoreactivity after the reperfusion, and they had no positive cell in TUNEL stain. In the 2-hour ischemia group, the keratinocytes gradually increased the reactivity for HSP72; consequently they also had no positive cell in TUNEL stain at all. In the 8-hour ischemia group, the reactivity for HSP72 was revealed at 8 hours after the reperfusion and suddenly decreased at 24 hour after the reperfusion; consequently they revealed positive for TUNEL stain. And they also expressed active form of caspase-3 at 8 hours after the reperfusion.We concluded that these differences of HSP72 expression were related to the deep follicle''s vulnerability to ischemia. The 8-hour ischemia induced the disturbance of HSP72 induction only in the deep hair follicles, consequently the keratinocytes in the deep hair follicles revealed apoptosis. And this apoptosis was accompanied with the activation of caspase-3. Less