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1 Although capsaicin analogs might be a potential strategy to manipulate inflammation, the mechanism is still unclear. In this study, the effects and action mechanisms of vanilloid analogs on iNOS and COX-2 expression were investigated in RAW264.7 macrophages. 2 Capsaicin and resiniferatoxin (RTX) can inhibit LPS-and IFN-g-mediated NO production, and iNOS protein and mRNA expression with similar IC 50 values of around 10 mM. 3 Capsaicin also transcriptionally inhibited LPS-and PMA-induced COX-2 expression and PGE 2 production. However, this effect exhibited a higher potency (IC 50 : 0.2 mM), and RTX failed to elicit such responses at 10 mM. 4 Interestingly, we found that capsazepine, a competitive TRPV1 antagonist, did not prevent the inhibition elicited by capsaicin or RTX. Nevertheless, it mimicked vanilloids in inhibiting iNOS/NO and COX-2/PGE 2 induction with an IC 50 value of 3 mM. RT -PCR and immunoblotting analysis excluded the expression of TRPV1 in RAW264.7 macrophages. 5 The DNA binding assay demonstrated the abilities of vanilloids to inhibit LPS-elicited NF-kB and AP-1 activation and IFN-g-elicited STAT1 activation. The reporter assay of AP-1 activity also supported this action. 6 The kinase assay indicated that ERK, JNK, and IKK activation by LPS were inhibited by vanilloids. 7 In conclusion, vanilloids can modulate the expression of inflammatory iNOS and COX-2 genes in macrophages through interference with upstream signalling events of LPS and IFN-g. These findings provide new insights into the potential benefits of the active ingredient in hot chilli peppers in inflammatory conditions.

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A Rhodobacter sphaeroides WL-APD911 with the capability of producing the end products of neurosporene and ξ-carotene, rather than the normal end products of spheroidene, was isolated from hundreds of strains by using chemical mutagenesis. The strain WL-APD911 grew well in LB medium, and the colored carotenoids were produced within 3 days of incubation at 30°C. The Rs-M of colored carotenoid extracts obtained from strain WL-APD911 by using methanol extraction inhibited the NO production and iNOS expression by LPS-induced RAW 264.7 cells. This probability of reason for the Rs-M as the best source was to prompt the anti-inflammation and anti-oxidation in nutraceutical products. Finally, the carotenoid extracts (Rs-M) with neurosporene and ξ-carotene was called lycogene to be a newly biomaterial.

Methyl gallate is a polyphenolic compound found in many plants, and its antioxidant, antitumor, antibacterial, and anti-inflammatory effects have been extensively studied. More recently, antidepressant-like effects of methyl gallate have been demonstrated in some studies. In the present study, we examined the effects of methyl gallate on melanogenesis, including the tyrosinase inhibitory effect, the melanin content, and the molecular signaling pathways involved in this inhibition. The results showed that methyl gallate inhibited tyrosinase activity and significantly downregulated the expressions of melanin synthesis-associated proteins, including microphthalmia-associated transcription factor (MITF), tyrosinase, dopachrome tautomerase (Dct), and tyrosinase-related protein-1 (TRP1). In conclusion, our findings indicated that activation of MEK/ERK and PI3K/Akt promoted by methyl gallate caused downregulation of MITF and triggered its downstream signaling pathway, thereby inhibiting the production of melanin. In summary, methyl gallate showed significant inhibitory activity against melanin formation, implying that it may be a potential ingredient for application in skin-whitening cosmetics.