Coompo Research Chemicals

Enhanced oxidative stress and inflammation play important roles in the pathogenesis of Alzheimer's disease (AD). Amyloid β-peptide (Aβ), a major component of amyloid plaques, is considered to have a causal role in the development and progress of AD by being the initiator of a pathological cascade leading to oxidative stress. The present study investigated the effect of N-trans-feruloyltyramine (NTF)shown to protect against oxidative stress and cell death. Pre-treatment of rat primary cortical cell cultures with 25-250μM NTF significantly attenuated 10μM Aβ(1-42)-induced neuronal death in a dose-dependent manner. Apoptotic cell death was demonstrated morphologically as well as by detection of the presence of activated caspase-3 and Bax, levels of which could be reduced by NTF pre-treatment. NTF also reduced production of reactive oxygen species induced by Aβ(1-42). These findings suggest that the protective effect of NTF against Aβ(1-42)-induced neuronal death might be due to its antioxidative property.

At the concentration of 0.05 μM, NTF was able to suppress P-selectin expression on platelets by 31% (P < 0.016). Since COX enzymes are deeply involved in the regulation of P-selectin expression on platelets, potential effects of NTF on COX enzymes were investigated. As expected at the concentration of 0.05 μM, NTF was found to be a very potent compound able to inhibit COX-I and -II enzymes by 43% (P < 0.012) and 33% (P < 0.014), respectively. NTF is likely to inhibit COX enzymes, thereby suppressing P-selectin expression on platelets.

Melanogenesis was inhibited by NTF in a dose-dependent manner. NTF exhibited a greater potency than kojic acid as a standard inhibitor of melanogenesis. Moreover, treatment of B16 melanoma cells with NTF was found to cause marked decreases in the expression levels of tyrosinase. NTF -induced downregulation of tyrosinase resulted in suppression of melanin biosynthesis in murine B16 melanoma cells.