. Author manuscript; available in PMC: 2017 Jun 21.

Published in final edited form as: Ann N Y Acad Sci. 2016 Jun 21;1374(1):184–192. doi: 10.1111/nyas.13099

Table 1.

Effect of silibinin on CEES- or NM-induced injury end points in skin epidermal cells, skin fibroblasts, or SKH-1 hairless mice

Injury end point	Model and vesicant	Effect of silibinin
Cell viability	Skin epidermal cells and fibroblast models with CEES	Decreases the CEES-induced Increase⁴²
Apoptotic cell death	Skin epidermal cells and fibroblast models with CEES SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70
Cellular and mitochondrial oxidative stress	Skin epidermal cells and fibroblast models with CEES	Decreases the CEES-induced increase⁴²
Skin epidermal thickness, denuding, or other changes	SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70
Microvesication	SKH-1 hairless mouse skin injury model with NM	Decrease in NM-induced increase⁷⁰
Myeloperoxidase activity	SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70
DNA damage (H2A.X or p53 phosphorylation)	Skin epidermal cells and fibroblast models with CEES SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70
Inflammatory and proteolytic mediators (COX-2, iNOS, MMP9)	SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70
Transcription factors AP-1 and NF-κB	SKH-1 hairless mouse skin injury model with CEES	Decreases the CEES-induced increase⁴²
Lipid peroxidation, protein oxidation, and oxidative DNA damage	SKH-1 hairless mouse skin injury model with CEES and NM	Decreases the CEES- and NM- induced increase^42,70