Costa Adilson, Facchini Gustavo, Pinheiro Ana Lúcia T A, da Silva Michelle S, Bonner Michael Y, Arbiser Jack, Eberlin Samara
Department of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, Winship Cancer Institute, Atlanta, GA, USA.
KOLderma Clinical Trials Institute - Kosmoscience Group, Campinas, SP, Brazil.
Int J Dermatol. 2017 Jul;56(7):754-761. doi: 10.1111/ijd.13569. Epub 2017 Feb 22.
Pollution, especially cigarette smoke, is a major cause of skin damage.
To assess the effects of the small molecule polyphenol, honokiol, on reversing cigarette smoke-induced damage in vitro to relevant skin cells.
Keratinocytes (HaCat) cultures were exposed to cigarette smoke and, after 48 hours, IL-1α and IL-8 were measured in cell supernatants. Moreover, TIMP-2 production, apoptosis rate, and senescence β-galactosidase expression were evaluated in primary human foreskin fibroblasts (HFF-1) cultures.
Honokiol at 10 μm reduced IL-1α production by 3.4 folds (P < 0.05) and at 10 and 20 μm reduced IL-8 by 23.9% and 53.1% (P < 0.001), respectively, in HaCat keratinocytes. In HFF-1, honokiol restored TIMP-2 production by 96.9% and 91.9% (P < 0.001), respectively, at 10 and 20 μm, as well as reduced apoptosis by 47.1% (P < 0.001) and 41.3% (P < 0.01), respectively. Finally, honokiol reduced senescence-associated β-galactosidase expression in HFF-1.
Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.
污染，尤其是香烟烟雾，是皮肤损伤的主要原因。
评估小分子多酚厚朴酚对体外逆转香烟烟雾诱导的相关皮肤细胞损伤的作用。
将角质形成细胞（HaCat）培养物暴露于香烟烟雾中，48小时后，测量细胞上清液中的白细胞介素-1α（IL-1α）和白细胞介素-8（IL-8）。此外，在原代人包皮成纤维细胞（HFF-1）培养物中评估金属蛋白酶组织抑制因子-2（TIMP-2）的产生、凋亡率和衰老β-半乳糖苷酶表达。
在HaCat角质形成细胞中，10μm的厚朴酚使IL-1α的产生减少3.4倍（P<0.05），10μm和20μm的厚朴酚分别使IL-8减少23.9%和53.1%（P<0.001）。在HFF-1中，10μm和20μm的厚朴酚分别使TIMP-2的产生恢复96.9%和91.9%（P<0.001），同时分别使细胞凋亡减少47.1%（P<0.001）和41.3%（P<0.01）。最后，厚朴酚降低了HFF-1中衰老相关β-半乳糖苷酶的表达。
厚朴酚可保护HFF-1和HaCat免受香烟烟雾诱导的炎症、胶原分解、细胞凋亡和衰老。
