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AdiponinTM, an INCI named cosmeceutical / cosmetic ingredient (SE214), is a low molecular-weight tripeptide derived from Adiponectin, an adipose-tissue specific releasing adipokine. This protein circulates through the human body and suppresses not only inflammatory reaction and carcinogenic metastasis, but also works for skin regeneration, moisturization and wrinkle enhancement.

 

 

- Adiponectin facilitates the proliferation of keratinocytes and fibroblasts, induces the generation of extracellular matrix (ECM) like collagen and facilitates the expression of fillaggrin while adiponectin heals the damaged skin, suppresses fibrosis, enhances the wrinkles and forms the skin barrier, moisturizing the skin.

 

- In addition, adiponectin enhances insulin sensitivity and improves insulin resistance, which leads to amelioration of the cardiovascular diseases like hyperglycemia, hyperinsulinemia, obesity and atherosclerosis. Adiponectin also suppresses the metastasis of cancer cells and inflammatory reactions.

 

 

  1. The proliferation of Cultured mouse fibroblast ( NIH3T3)

     

    - The proliferation of the fibroblasts was observed to be significantly enhanced by Adiponin.

     

  2. The activated expression of Procollagen Type-1 in fibroblasts

     

    - Adiponin dose-dependently induced the expression of type 1 procollagen in human dermal fibroblasts.

     

  3. The expression of skin-barrier related protein in cultured human keratinocyte HaCaT cell line.

     

    - Adiponin treatment upregulated the expression of the skin-barrier forming Profillagrin, Involucrin and Ioricrin dose-dependently.

     

     

     

     

  4. Suppression of the activation of the inflammatory transcription factor, NF-κB

     

    - Dose-dependent treatment with adiponin significantly inhibited the activation of proinflammatory transcription factor NF-κB, which was induced by TNFα.

     

     

     

  5. In vitro suppression of the extravasation of monocytes

     

    - Adipoinin treatment prominently suppressed the extravasation of monocytes U937 through the Human Umbilical Vein Endothelial Cell layer.

     

     

     

     

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