Not marketing claims — the underlying mechanisms, with citations. Here's what happens at the cellular level when this formula meets your skin.
Vitamin A is abundant in unrefined shea butter. Vitamin A and its derivatives (retinoids) are fundamental to the regulation of skin cell activity. Retinoids bind to specific nuclear receptors (RARs and RXRs) within keratinocytes, acting as transcription factors that regulate cell proliferation, differentiation, and apoptosis.
Studies using 3D human-equivalent skin models indicate that retinoid formulations can accelerate wound closure by stimulating fibroblast activity and modulating the collagen matrix, supporting better tissue stratification and structural remodeling.
Vitamin E is abundant in unrefined shea butter. Vitamin E (tocopherol) serves as the primary lipid-soluble antioxidant in the skin's protective barrier. The skin's lipid matrix is susceptible to oxidative damage, which can lead to inflammation and compromised barrier function. Vitamin E effectively sequesters free radicals within cell membranes, preventing lipid peroxidation and maintaining the integrity of the stratum corneum.
Vitamin E works in concert with other antioxidants, including polyphenols, to mitigate oxidative stress. By stabilizing the lipid barrier, it helps prevent transepidermal water loss and protects against UV-induced damage, providing a stable environment for skin recovery.
Green Tea contains a large amount of epigallocatechin gallate (EGCG), a powerful antioxidant with strong anti-inflammatory and antimicrobial properties. EGCG neutralizes free radicals that cause lipid, protein, and DNA damage.
EGCG also upregulates the body's own internal defense system by activating the Keap1/Nrf2 pathway. When Nrf2 is activated, it travels to the cell nucleus and triggers the production of natural antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase.
The calming effect of green tea on irritated skin is primarily due to its role as a potent inhibitor of the NF-κB (nuclear factor-kappa B) signaling pathway. In a resting state, NF-κB is held inactive in the cytoplasm by a protein called IκB.
When the skin experiences trauma (like a new tattoo), inflammatory signals trigger the IKK (IκB kinase) complex. IKK phosphorylates IκB, causing it to degrade and releasing NF-κB. Once freed, NF-κB enters the nucleus and acts as a master switch to turn on pro-inflammatory genes (cytokines like TNF-α, IL-1β, and IL-6).
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Keen, M. A., & Hassan, I. (2016). Vitamin E in dermatology. Indian Dermatology Online Journal, 7(4), 311–315. https://doi.org/10.4103/2229-5178.185494
Liu, D., Perkins, J. T., & Hennig, B. (2016). EGCG prevents PCB-126-induced endothelial cell inflammation via epigenetic modifications of NF-κB target genes in human endothelial cells. The Journal of Nutritional Biochemistry, 28, 164–170. https://doi.org/10.1016/j.jnutbio.2015.10.003
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Niu, L. (2026). Dietary (−)-epigallocatechin gallate (EGCG): State-of-the-art advances in bioactivities, bioavailability enhancement strategies, and applications in nutrition and health. Nutrients, 18(2), 317.
Pincemail, J., & Meziane, S. (2022). On the potential role of the antioxidant couple vitamin E/selenium taken by the oral route in skin and hair health. Antioxidants, 11(11), 2270. https://doi.org/10.3390/antiox11112270
Sun, J., Jiang, Y., Fu, J., He, L., Guo, X., Ye, H., Yin, C., Li, H., & Jiang, H. (2024). Beneficial effects of epigallocatechin gallate in preventing skin photoaging: A review. Molecules, 29(22), 5226. https://doi.org/10.3390/molecules29225226
Zasada, M., & Budzisz, E. (2019). Retinoids: Active molecules influencing skin structure formation in cosmetic and dermatological treatments. Advances in Dermatology and Allergology, 36(4), 392–397. https://doi.org/10.5114/ada.2019.87443
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