Centella AsiaticavsCeramides

The four key triterpenoid saponins—madecassoside, asiaticoside, madecassic acid, and asiatic acid—exert distinct but complementary mechanisms. Madecassoside and asiaticoside are anti-inflammatory: they inhibit NF-κB nuclear translocation and IκB kinase activity, reducing TNF-α, IL-6, and IL-1β production in keratinocytes and dermal cells. Madecassic acid and asiatic acid (the aglycone forms) stimulate type I and III collagen synthesis in fibroblasts by upregulating collagen gene expression and procollagen production. All four compounds promote wound healing by stimulating angiogenesis via VEGF (vascular endothelial growth factor) upregulation, fibroblast proliferation and migration, and extracellular matrix remodeling. Centella extracts also increase superoxide dismutase (SOD) and catalase activity in skin cells, enhancing endogenous antioxidant defense. The triterpenes may modulate TGF-β and Smad signaling. TECA (Titrated Extract of Centella Asiatica) standardizes these actives for consistent clinical efficacy.

Ceramides are sphingolipids comprising a sphingoid base (sphingosine or phytosphingosine) amide-linked to a fatty acid—comprising ~50% of stratum corneum lipids. They integrate into the intercellular lipid matrix between corneocytes, forming the lamellar bilayer structure with cholesterol and free fatty acids that limits transepidermal water loss (TEWL). Optimal molar ratio is ~3:1:1 (ceramides:cholesterol:fatty acids). Topical ceramides (NP/3, AP/6-II, EOP/1) fill gaps from barrier damage by surfactants, retinoids, or inflammation. Cholesterol enables lamellar phase formation; fatty acids provide acidic pH for ceramide packing. Products restoring the complete ratio upregulate barrier repair genes (involucrin, filaggrin, transglutaminase) more effectively. Synthesis occurs via serine palmitoyltransferase and ceramide synthase in keratinocytes.