The oxidative stress corresponds to an imbalance between the production of free radicals and the skin’s antioxidant defenses.
Generated under the influence of UV rays, pollution, smoking, or even cellular metabolism, free radicals can accumulate in the skin and damage lipids, proteins, and cellular DNA. In the long term, this phenomenon contributes to the degradation of the dermal matrix, the reduction of cellular repair capacity, and to the acceleration of skin aging, which is why it is important to incorporate antioxidants into your skincare routine.
The Centella asiatica exhibits a well-documented antioxidant activity, which is often cited as one of gotu kola’s main benefits for the skin, especially when it is exposed daily to environmental stressors. These effects are largely attributed to its triterpenes, particularly asiatic acid. These compounds are able to directly reduce free radical production and lipid peroxidation, while restoring endogenous antioxidant defenses. More specifically, asiatic acid activates the Nrf2 signaling pathway, notably via the Akt and ERK pathways, resulting in increased expression of enzymes involved in the antioxidant response—such as heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase-1 (NQO1), and glutamyl-cysteine ligase. Concurrently, these triterpenes limit the production of pro-oxidant and pro-inflammatory mediators like nitric oxide, TNF-α, and IL-6, thereby indirectly reducing the oxidative load within skin tissues.
This antioxidant activity was demonstrated in a study conducted on human dermal fibroblasts subjected to oxidative stress induced by hydrogen peroxide (H₂O₂). Pretreatment of the fibroblasts with various concentrations of Centella asiatica extract (15–60 µg/mL) significantly attenuated H₂O₂-induced cytotoxicity. Gene expression analyses revealed a marked increase in cellular antioxidant enzymes, notably catalase (CAT) and superoxide dismutases 1 and 2 (SOD1, SOD2). This was accompanied by inhibition of matrix metalloproteinase MMP-9, an enzyme involved in extracellular matrix degradation under oxidative stress conditions.