Abstract
The big belly seahorse (Hippocampus abdominalis), a well-known ingredient of traditional medicine, possesses anti-inflammatory, anti-aging, anti-fatigue, and anti-thrombotic properties, and also increases male fertility. This study demonstrates that the ethanolic extract of dried H. abdominalis (EEHA) has anti-melanogenic effects in B16F10 melanoma cells and zebrafish larvae. EEHA significantly reduced the α-melanocyte-stimulating hormone (α-MSH)-induced melanogenesis in B16F10 melanoma cells without causing cytotoxicity. At a concentration of 200 µg/mL, EEHA had significant anti-melanogenic activity in zebrafish larvae, accompanied by a severe reduction in the heart rate (118 ± 17 heartbeats/min) compared to that of the untreated group (185 ± 8 heartbeats/min), indicating that EEHA induces cardiotoxicity at high concentrations. Below 100 µg/mL, EEHA significantly reduced melanogenesis in zebrafish larvae in the presence or absence of α-MSH, while the heart rate remained unaltered. Additionally, EEHA downregulated the release of cyclic adenosine monophosphate (cAMP) and the phosphorylation of cAMP response element-binding protein (CREB) in B16F10 melanoma cells, which inhibited microphthalmia-associated transcription factor (MITF), leading to the inhibition of tyrosinase activity. EEHA also increased the phosphorylation of extracellular-signal regulated kinase (ERK). The ERK inhibitor PD98059 interfered with the anti-melanogenic activity of EEHA in B16F10 melanoma cells and zebrafish larvae, indicating that the ERK signaling pathway might regulate the anti-melanogenic properties of EEHA. Altogether, we conclude that EEHA represses the cAMP–CREB–MITF axis, which consequently inhibits tyrosinase-mediated melanogenesis. We propose that at low concentrations, EEHA can serve as a promising anti-melanogenic agent that could be used to prepare whitening cosmetics and for treating melanogenic disorders.
Highlights
The primary biological function of synthesized melanin is to protect the skin from ultraviolet (UV)radiation and reactive free radicals [1]
Since the upregulation of cyclic adenosine monophosphate (cAMP) is directly of 200 μg/mL, extract of dried H. abdominalis (EEHA) downregulated the levels of phosphorylated cAMP response element-binding protein (CREB) in B16F10 melanoma cells by associated with the phosphorylation of CREB, we evaluated the effect of EEHA on CREB
Our findings demonstrated that the melanogenesis mediated by α-melanocyte-stimulating hormone (α-MSH) in B16F10 melanoma cells
Summary
The primary biological function of synthesized melanin is to protect the skin from ultraviolet (UV)radiation and reactive free radicals [1]. Α-MSH leads to melanin biosynthesis by upregulating microphthalmia-associated transcription factor (MITF), which activates tyrosinase, a key copper-containing enzyme that catalyzes the two rate-limiting steps of melanogenesis, namely, the hydroxylation of tyrosine to 3,4-dihydroxyphenylalanine (l-DOPA), and the oxidation of l-DOPA to dopaquinone [6]. It has been recently identified that proteins belonging to the mitogen-activated protein kinase (MAPK) family, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK, regulate melanogenesis by modulating the expression of tyrosinase. The phosphorylation of ERK and JNK has been found to induce the degradation of MITF that is mediated by ubiquitination, which subsequently inhibits the expression of tyrosinase, thereby inducing anti-melanogenesis. Numerous inhibitors of p38 MAPK and/or activators that target ERK and JNK have, been developed as anti-melanogenic agents
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