Glucocorticoid(GC) is a stress-related hormone that affects hair follicle(HF) function and growth cycle regulation, and is converted from inactive cortisone to active cortisol by 11β-Hydroxysteroid dehydrogenase type1(11β-HSD1). Recent studies have shown that the expression of 11β-HSD1 in human hair follicles and the negative effects of glucocorticoids on Dermal papilla cell(DPC) can be prevented by inhibiting 11β-HSD1. This suggests that 11β-HSD1 inhibitors can be applied to the treatment of stress-related hair loss. However, in stress environment the effects of 11β-HSD1 inhibitors remained unclear in human hair follicles and their cells.We treated cortisone and UVB to create a stress environment in human hair follicles, DPC, and Outer root sheath cell(ORSC). And we investigated the 11β-HSD1 inhibitory effect of NTX-101.11β-HSD1 mRNA levels upregulated by cortisone/UVB were suppressed by NTX-101 treatment in ORSC but not DPC. In addition, reduced cell proliferation by cortisone/UVB treatment was recovered by NTX-101 direct treatment in ORSC and NTX-101 treated ORSC supernatant restored DPC proliferation through induce of Wnt3A, β-catenin and Ki-67 protein. Hair follicle elongation inhibited by cortisone/UVB exposure was restored by NTX-101, and Wnt3A and Ki-67 expression was up-regulation.In this study, we demonstrated that 11β-HSD1 inhibitor regulated hair growth under cortisone/UVB exposed stressful environment in an ex vivo system and an in vitro model using Dermal papilla cells(DPCs) and Outer root sheath cells(ORSCs). It was confirmed that the 11β-HSD1 inhibitor regulates hair follicle growth through the regulation of the Wnt/β-catenin signaling pathway. From these results, we propose that an 11β-HSD1 inhibitor could be used for stress-induced hair disorder.