Stress alters cutaneous permeability barrier homeostasis
Stress alters cutaneous permeability barrier homeostasis
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DOI：
10.1152/ajpregu.2000.278.2.r367
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发表时间：
2000-02-01
影响因子：
2.8
通讯作者：
Feingold, KR
中科院分区：
文献类型：
--
作者：
Denda, M;Tsuchiya, T;Feingold, KR
最近的研究表明，心理应激可以影响皮肤屏障的功能，这表明这种形式的应激可能触发或加重皮肤病；在本研究中，我们证明了将无毛小鼠转移到不同的笼子会延迟屏障恢复的速度。在动物移植之前，预先给予吩噻嗪镇静剂氯丙嗪，使屏障恢复的动力学恢复到正常，这表明心理应激是屏障稳态改变的基础。为了确定心理应激与改变的屏障恢复之间的联系机制，我们首先证明了将动物转移到新笼子后血浆皮质酮水平显著升高，并用氯丙嗪预先阻断了这种增加，其次，我们证明了全身应用皮质酮延迟了屏障恢复。最后，我们证明用糖皮质激素受体拮抗剂RU-486预处理可阻断全身皮质酮、更换CAGE或制动所产生的屏障恢复延迟。这些结果表明，心理应激刺激糖皮质激素的产生增加，而糖皮质激素反过来又对通透性屏障的动态平衡产生不利影响。
Recent studies have shown that psychological stress can influence cutaneous barrier: function, suggesting that this form of stress could trigger or aggravate skin disease; In the present study, we demonstrate that transfer of hairless mice to a different cage delays barrier recovery rates. Pretreatment with a phenothiazine sedative, chlorpromazine, before transfer of animals restored the kinetics of barrier recovery toward normal, suggesting that psychological stress is the basis for this alteration in barrier homeostasis. To determine the mechanism linking psychological stress to altered barrier recovery, we first-demonstrated that plasma corticosterone levels increase markedly after transfer of animals to new cages and that pretreatment with chlorpromazine blocks this increase, Second, we demonstrated that the systemic administration of corticosterone delays barrier recovery. Finally, we demonstrated that pretreatment with the glucocorticoid receptor antagonist RU-486 blocks the delay in barrier recovery produced by systemic corticosterone, change of cage, or immobilization. These results suggest that psychological stress:stimulates increased production of glucocorticoids, which, in turn, adversely affects permeability barrier homeostasis.