Kaempferol Blocks the Skin Fibroblastic Interleukin 1β Expression and Cytotoxicity Induced by 12-O-tetradecanoylphorbol-13-acetate by Suppressing c-Jun N-terminal Kinase

Nutrients

Su-Ji Park¹  Do-Wan Kim¹  Seong-Ryeong Lim¹  Sei-Jung Lee¹  Chang-Hyung Choi²  Tae Hoon Kim³  In Sun Min⁴  Junghee Sung⁵ 

[1] Department of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, Korea;Division of Cosmetic Science and Technology, Daegu Haany University, Gyeongsan 38610, Korea;FoodyWorm Inc., Yancheongsongdae-gil 10, Ochang-eup, Cheongwon-gu, Choenju-si 28118, Korea;Fragrance of the Moon, 23 Taepyeong-ro, Jung-gu, Daegu 41900, Korea;Research Center, Reanzen Co., Ltd., Anyang 14056, Korea;

关键词: 12-O-tetradecanoylphorbol 13-acetate;    apoptosis;    kaempferol;    normal human dermal fibroblast;    reactive oxygen species;   

DOI  :  10.3390/nu13093079

来源: DOAJ

【 摘 要 】

Kaempferol, a bioflavonoid present in fruits and vegetables, has a variety of antioxidant and anti-inflammatory capacities, but the functional role of kaempferol in oxidative skin dermal damage has yet to be well studied. In this study, we examine the role of kaempferol during the inflammation and cell death caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human dermal fibroblasts (NHDF). TPA (5 μM) significantly induced cytotoxicity of NHDF, where a robust increase in the interleukin (IL)-1β mRNA among the various pro-inflammatory cytokines. The skin fibroblastic cytotoxicity and IL-1β expression induced by TPA were significantly ameliorated by a treatment with 100 nM of kaempferol. Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Interestingly, we found that kaempferol inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and the inhibitor NF-κB (IκBα), which are necessary for the expression of cleaved caspase-3 and the IL-1β secretion in TPA-treated NHDF. These results suggest that kaempferol is a functional agent that blocks the signaling cascade of the skin fibroblastic inflammatory response and cytotoxicity triggered by TPA.

【 授权许可】

Unknown