Detroit 551

Expression of Collagen on Ac2-26 Treated Human Fibroblast Cells

Skin inflammation is a prevalent dermatological issue, and the anti-inflammatory responses of skin cells are crucial for combating these conditions. Annexin A1 (AnxA1) is a well-characterized endogenous anti-inflammatory mediator. However, the function of AnxA1 in skin keratinocytes and fibroblasts remains poorly understood. Kim et al. explored whether AnxA1 mimetic peptide Ac2-26 had anti-inflammatory and anti-wrinkle properties in human keratinocyte (HaCaT) and fibroblast (Detroit 551) cells.

They explored the effects of Ac2-26 on anti-wrinkle proteins in human fibroblast Detroit 551 cells. Cell viability assay (Fig. 1A) showed that there was no cytotoxic effect in 1, 5, and 10 ng/mL Ac2-26, and these doses were used for subsequent studies. As wrinkle formation is caused by low levels of collagen in the dermis, they next measured the secretion of procollagen, a precursor of collagen, in Ac2-26-treated Detroit 551 cells. The results (Fig. 1B) showed that Ac2-26 increased procollagen levels, and this implies that Ac2-26 induced collagen synthesis. Next, they measured the expression of collagenase proteins including MMP-1, MMP-8, and COL1A1. Figure 1C shows that Ac2-26 significantly inhibited MMP-1 and MMP-8, and increased COL1A1 levels. These results suggest that Ac2-26 promotes collagen synthesis and inhibits collagen degradation in Detroit 551 cells.

Effects of Luffa Cylindrica Stem Sap (LuCS) Treatment on Cellular Procollagen or Elastin Expression in Human Fibroblasts

Luffa cylindrica stem sap (LuCS) has been ethnopharmacologically used as a cosmetic ingredients to improve the facial condition in Asians, but there is no scientific proof about the advantages of LuCS as a supplement for skin elasticity inducer. Previously, Lee et al. have reported that the functional effects of LuCS on human skin are associated with regulating elastin and type I pro-collagen in human fibroblasts against intrinsic and extrinsic cues through the EGFR and PPARγ signaling. To further validate the effect of LuCS exposure on cellular elastin and collagen type I expression in human fibroblast, they performed Western blot analysis using LuCS treated Detroit-551 cells. Exposure to LuCS dose-dependently induced the expression of type I procollagen in Detroit-551 cells (Fig. 2A). LuCS treatment also significantly stimulated the expression of elastin in Detroit-551 cells in a dose-dependnet manner (Fig. 2B).