Virgin coconut oil (VCO) has been traditionally used as moisturizer since centuries by people in the tropical region. Clinical studies have revealed that VCO improves the symptoms of skin disorders by moisturizing and soothing the skin. However, the mechanistic action of VCO and its benefits on skin has not been elucidated in vitro. The cytotoxicity (CTC50) of VCO was 706.53 ± 2.1 and 787.15 ± 1.1 μg/mL in THP-1 (Human monocytes) and HaCaT (Human keratinocytes) cells respectively. VCO inhibited TNF-α (62.34 ± 3.2 %), IFN-γ (42.66 ± 2.9 %), IL-6 (52.07 ± 2.0 %), IL-8 (53.98 ± 1.8 %) and IL-5 (51.57 ± 2.6 %) respectively in THP-1 cells. Involucrin (INV) and filaggrin (FLG) content increased by 47.53 ± 2.1 % and 40.45 ± 1.2 % respectively in HaCaT cells. VCO increased the expression of Aquaporin-3 (AQP3), involucrin (INV) and filaggrin (FLG) and showed moderate UV protection in HaCaT cells. In vitro skin irritation studies in Reconstructed human epidermis (RHE) and NIH3T3 cells showed that VCO is a non skin irritant (IC50 > 1000 μg/mL) and non phototoxic (PIF < 2). Our study demonstrated the anti inflammatory activity of VCO by suppressing inflammatory markers and protecting the skin by enhancing skin barrier function. This is the first report on anti-inflammatory and skin protective benefits of VCO in vitro. Overall, the results warrant the use of VCO in skin care formulations.

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Human skin is body’s vital organ constantly exposed to abiotic oxidative stress. This can have deleterious effects on skin such as darkening, skin damage, and aging. Plant-derived products having skin-protective effects are well-known traditionally. Triphala, a formulation of three fruit products, is one of the most important rasayana drugs used in Ayurveda. Several skin care products based on Triphala are available that claim its protective effects on facial skin. However, the skin protective effects of Triphala extract (TE) and its mechanistic action on skin cells have not been elucidated in vitro. Gallic acid, ellagic acid, and chebulinic acid were deduced by LC-MS as the major constituents of TE. The identified key compounds were docked with skin-related proteins to predict their binding affinity. The IC50 values for TE on human dermal fibroblasts (HDF) and human keratinocytes (HaCaT) were 204.90 ± 7.6 and 239.13 ± 4.3 μg/mL respectively. The antioxidant capacity of TE was 481.33 ± 1.5 mM Trolox equivalents in HaCaT cells. Triphala extract inhibited hydrogen peroxide (H2O2) induced RBC haemolysis (IC50 64.95 μg/mL), nitric oxide production by 48.62 ± 2.2%, and showed high reducing power activity. TE also rescued HDF from H2O2-induced damage; inhibited H2O2 induced cellular senescence and protected HDF from DNA damage. TE increased collagen-I, involucrin and filaggrin synthesis by 70.72 ± 2.3%, 67.61 ± 2.1% and 51.91 ± 3.5% in HDF or HaCaT cells respectively. TE also exhibited anti-tyrosinase and melanin inhibition properties in a dose-dependent manner. TE increased the mRNA expression of collagen-I, elastin, superoxide dismutase (SOD-2), aquaporin-3 (AQP-3), filaggrin, involucrin, transglutaminase in HDF or HaCaT cells, and decreased the mRNA levels of tyrosinase in B16F10 cells. Thus, Triphala exhibits protective benefits on skin cells in vitro and can be used as a potential ingredient in skin care formulations.

Liver is a prime target of alcohol-induced damage by inducing inflammatory cytokines especially tumor necrosis factor alpha (TNFalpha). Activator of peroxisome proliferator activator receptor gamma (PPARgamma) is protective against alcohol-induced liver injury in animals. Liv.52, one of the major herbal hepatoprotective drugs, is shown to protect the liver from toxicity and is considered to be an effective hepatoprotective agent. However, the signal pathway involved in the Liv.52-induced hepatoprotection is not understood well especially in the case of cultured liver cells treated with ethanol. Hence, the study was aimed at determining whether ethanol and Liv.52 could modulate PPARgamma and TNFalpha induction in human hepatoma cells, HepG2. The present study with RT-PCR and confocal microscopy experiments showed that ethanol (100 mM) induced suppression of PPARgamma expression in HepG2 cells. The ethanol-induced PPARgamma suppression was abrogated by Liv.52. Moreover, Liv.52 also induced upregulation of PPARgamma mRNA in liver cells as compared to the untreated cells. Further, 100 mM ethanol has also induced TNFalpha gene expression in HepG2 cells and interestingly Liv.52 abolished ethanol-induced TNFalpha. The study also shows that Liv.52 alone downregulated TNFalpha expression in HepG2 cells. Taken together, these findings suggest that Liv.52 is capable of attenuating ethanol-induced expression of TNFalpha and abrogating ethanol-induced suppression of PPARgamma in liver cells. These results indicate that Liv.52-induced PPARgamma expression and concomitant suppression of ethanol-induced elevation of TNFalpha in HepG2 cells suggest the immunomodulatory and hepatoprotective nature of Liv.52.

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