Tyrosinase inhibitors have become increasingly important targets for hyperpigmentation disease treatment. Kojic monooleate (KMO), synthesized from the esterification of kojic acid and oleic acid, has shown a better depigmenting effect than kojic acid. In this study, the process parameters include the speed of high shear, the time of high shear and the speed of the stirrer in the production of nanoemulsion containing KMO was optimized using Response Surface Methodology (RSM), as well as evaluated in terms of its physicochemical properties, safety and efficacy. The optimized condition for the formulation of KMO nanoemulsion was 8.04 min (time of high shear), 4905.42 rpm (speed of high shear), and 271.77 rpm (speed of stirrer), which resulted in a droplet size of 103.97 nm. An analysis of variance (ANOVA) showed that the fitness of the quadratic polynomial fit the experimental data with large F-values (148.79) and small p-values (p < 0.0001) and an insignificant lack of fit. The optimized nanoemulsion containing KMO with a pH value of 5.75, showed a high conductivity value (3.98 mS/cm), which indicated that the nanoemulsion containing KMO was identified as an oil-in-water type of nanoemulsion. The nanoemulsion remains stable (no phase separation) under a centrifugation test and displays accelerated stability during storage at 4, 25 and 45 °C over 90 days. The cytotoxicity assay showed that the optimized nanoemulsion was less toxic, with a 50% inhibition of cell viability (IC50) > 500 μg/mL, and that it can inhibit 67.12% of tyrosinase activity. This study reveals that KMO is a promising candidate for the development of a safe cosmetic agent to prevent hyperpigmentation.
Emerging dye pollution from textile industrial effluents is becoming more challenging for researchers worldwide. The contamination of water by dye effluents affects the living organisms in an ecosystem. Methylene blue (MB) and malachite green (MG) are soluble dyes with a high colour intensity even at low concentration and are hazardous to living organisms. The adsorption method is used in most wastewater plants for the removal of organic pollutants as it is cost-effective, has a high adsorption capacity, and good mechanical stabilities. In this study, a composite adsorbent was prepared by impregnating iron modified silica (FMS) onto polyurethane (PU) foam to produce an iron modified silica/polyurethane (FMS/PU) composite. The composite adsorbent was utilised in batch adsorption of the cationic dyes MB and MG. The effect of adsorption parameters such as the adsorbent load, pH, initial dye concentration, and contact time were discussed. Adsorption kinetics and isotherm were implemented to understand the adsorption mechanism for both dyes. It was found that the adsorption of MB and MG followed the pseudo-second order model. The Langmuir model showed a better fit than the Freundlich model for the adsorption of MB and MG, indicating that the adsorption occurred via the monolayer adsorption system. The maximum adsorption capacity of the FMS/PU obtained for MB was 31.7 mg/g, while for MG, it was 34.3 mg/g. The thermodynamic study revealed that the adsorption of MB and MG were exothermic and spontaneous at room temperature. In addition, the regeneration of FMS/PU was conducted to investigate the composite efficiency in adsorbing dyes for several cycles. The results showed that the FMS/PU composite could be regenerated up to four times when the regeneration efficiency dropped drastically to less than 20.0%. The impregnation of FMS onto PU foam also minimised the adsorbent loss into the environment.
Recent evidence from in vitro and in vivo studies has shown that anthocyanins and anthocyanidins can reduce and inhibit the amyloid beta (Aβ) species, one of the hallmarks of Alzheimer's disease (AD). However, their inhibition mechanisms on Aβ species at molecular details remain elusive. Therefore, in the present study, molecular modelling methods were employed to investigate their inhibitory mechanisms on Aβ(1-42) peptide. The results highlighted that anthocyanidins effectively inhibited the conformational transitions of helices into beta-sheet (β-sheet) conformation within Aβ(1-42) peptide by two different mechanisms: 1) the obstruction of two terminals from coming into contact due to the binding of anthocyanidins with residues of N- and second hydrophobic core (SHC)-C-terminals, and 2) the prevention of the folding process due to the binding of anthocyanidin with the central polar (Asp23 and Lys28) and native helix (Asp23, Lys28, and Leu34) residues. These new findings on the inhibition of β-sheet formation by targeting both N- and SHC-C-terminals, and the long-established target, D23-K28 salt bridge residues, not with the conventional central hydrophobic core (CHC) as reported in the literature, might aid in designing more potent inhibitors for AD treatment.