Denda Mitsuhiro, Fuziwara Shigeyoshi, Inoue Kaori
Shiseido Research Center, Yokohama, Japan.
J Invest Dermatol. 2003 Jul;121(1):142-8. doi: 10.1046/j.1523-1747.2003.12310.x.
Effects of topical application of adrenergic receptor agonists and antagonists on epidermal barrier repair rate after barrier disruption were studied. Agonists and antagonists of beta1-adrenergic receptor did not affect the barrier repair rate. On the other hand, beta2-adrenergic receptor agonists, procaterol and alprenol, delayed barrier recovery and the beta2 receptor antagonist, ICI-118551, blocked the delay. Moreover, topical application of ICI-118551 or beta1,2 receptor antagonist, clenbuterol alone accelerated barrier recovery. Antagonists of alpha1 and alpha2 receptors did not affect barrier recovery. The delay of barrier repair induced by prodaterol hydrochloride was blocked by a voltage-gated calcium channel blocker, verapamil or nifedipine. In cultured human keratinocytes, procaterol increased the intracellular calcium concentration and the increase was blocked by ICI-118551 and also by verapamil or nifedipine. Topical application of ICI-118551 partially blocked the epidermal hyperplasia induced by acetone treatment under low environmental humidity. These results suggest that the beta2-adrenergic receptor is specifically associated with skin barrier homeostasis.
研究了局部应用肾上腺素能受体激动剂和拮抗剂对屏障破坏后表皮屏障修复率的影响。β1肾上腺素能受体激动剂和拮抗剂不影响屏障修复率。另一方面，β2肾上腺素能受体激动剂丙卡特罗和阿普洛尔延迟了屏障恢复，而β2受体拮抗剂ICI-118551可阻断这种延迟。此外，单独局部应用ICI-118551或β1,2受体拮抗剂克伦特罗可加速屏障恢复。α1和α2受体拮抗剂不影响屏障恢复。盐酸丙卡特罗诱导的屏障修复延迟被电压门控钙通道阻滞剂维拉帕米或硝苯地平阻断。在培养的人角质形成细胞中，丙卡特罗增加细胞内钙浓度，ICI-118551以及维拉帕米或硝苯地平可阻断这种增加。在低环境湿度下，局部应用ICI-118551可部分阻断丙酮处理诱导的表皮增生。这些结果表明，β2肾上腺素能受体与皮肤屏障稳态密切相关。
