Green Tea Extract (EGCG)vsResveratrol

EGCG scavenges ROS (superoxide, hydroxyl radical, peroxynitrite) and chelates iron/copper that catalyze Fenton reactions. Inhibits MMP-2 (gelatinase A) and MMP-9 (gelatinase B) that degrade collagen types I, III, IV and elastin in photoaged skin — these enzymes are UV-upregulated via AP-1 and NF-kappa B. Reduces sebum by inhibiting 5-alpha reductase type 1 (testosterone to DHT conversion in sebaceous glands). Anti-inflammatory: NF-kappa B inhibition (I-kappa B degradation prevention), COX-2 suppression, TNF-alpha/IL-1beta reduction. Promotes keratinocyte differentiation via involucrin and filaggrin upregulation. Catechol structure enables dual antioxidant and metal-chelating activity. Topical EGCG reduces UV-induced erythema and prevents collagen degradation when used before sun exposure.

Resveratrol activates SIRT1 (sirtuin 1), a NAD+-dependent deacetylase that deacetylates histones and non-histone targets including p53, FOXO transcription factors, and NF-κB, regulating cellular stress response, DNA repair, autophagy, and inflammatory pathways in keratinocytes and fibroblasts. It scavenges superoxide anion, hydroxyl radical, and metal-induced free radicals through its phenolic hydroxyl groups. Resveratrol inhibits NF-κB nuclear translocation and downstream cytokine production (TNF-α, IL-1β, IL-6), reducing UV-induced inflammation. It inhibits tyrosinase (mild brightening), matrix metalloproteinase-9 (MMP-9, gelatinase B) to prevent collagen and elastin breakdown, and AP-1 (c-Fos/c-Jun) to reduce photoaging-related gene expression. It may also activate Nrf2, upregulating antioxidant enzymes (HO-1, NQO1). Topical application achieves higher skin tissue concentrations than oral supplementation due to first-pass metabolism. Stability is improved in anhydrous or encapsulated formulations.