Annona squamosa L. leaves inhibit alpha‐melanocyte‐stimulating hormone (α‐MSH) stimulated melanogenesis via p38 signaling pathway in B16F10 melanoma cells

2019 ◽  
Vol 19 (7) ◽  
pp. 1785-1792
Author(s):  
Gyeong‐A Ko ◽  
Hye Rim Kang ◽  
Jeong Yong Moon ◽  
Meran Keshawa Ediriweera ◽  
Sangmi Eum ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Melanoma Cells ◽  
Annona Squamosa ◽  
B16f10 Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Melanoma Cells ◽  
Stimulating Hormone

scholarly journals Metabolomics Reveals the Alteration of Metabolic Pathway by Alpha-Melanocyte-Stimulating Hormone in B16F10 Melanoma Cells

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3384 ◽  
Author(s):  
Seung-Ho Seo ◽  
Jae Kwon Jo ◽  
Eun-Ju Kim ◽  
Seong-Eun Park ◽  
Seo Yeon Shin ◽  
...  
Keyword(s):  
Citric Acid ◽  
Metabolic Pathway ◽  
Metabolic Pathways ◽  
Skin Pigmentation ◽  
Principal Component ◽  
Melanoma Cells ◽  
B16f10 Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Melanoma Cells ◽  
Stimulating Hormone

The purpose of this study was to understand the changes of metabolic pathway induced by alpha-melanocyte-stimulating hormone (α-MSH) in B16F10 melanoma cells in an untargeted metabolomics approach. Cells were treated with 100 nM of α-MSH and then incubated for 48 h. α-MSH increased tyrosinase activity and melanin content by 56.5 and 61.7%, respectively, compared to untreated cells after 48 h of cultivation. The clear separation between groups was observed in the principal component analysis score plot, indicating that the levels of metabolites of melanoma cells were altered by treatment with α-MSH. Metabolic pathways affected by α-MSH were involved in some amino acid metabolisms. The increased levels of fumaric acid, malic acid, oxaloacetic acid and citric acid related to the citric acid cycle pathway after α-MSH treatment suggested enhanced energy metabolism. Metabolic pathways altered by α-MSH treatment can provide useful information to develop new skin pigmentation inhibitors or anti-obesity drugs.

scholarly journals Flavonoid Glycosides from Ziziphus jujuba var. inermis (Bunge) Rehder Seeds Inhibit α-Melanocyte-Stimulating Hormone-Mediated Melanogenesis

2021 ◽  
Vol 22 (14) ◽  
pp. 7701
Author(s):  
Ilandarage Menu Neelaka Molagoda ◽  
Kyoung-Tae Lee ◽  
Athapaththu Mudiyanselage Gihan Kavinda Athapaththu ◽  
Yung-Hyun Choi ◽  
Jaeyoung Hwang ◽  
...  
Keyword(s):  
Biological Activities ◽  
Melanoma Cells ◽  
Flavonoid Glycosides ◽  
B16f10 Melanoma ◽  
Anticancer Activities ◽  
Melanocyte Stimulating Hormone ◽  
Zebrafish Larvae ◽  
B16f10 Melanoma Cells ◽  
Ziziphus Jujuba ◽  
Stimulating Hormone

Ziziphus jujuba extracts possess a broad spectrum of biological activities, such as antioxidant and anticancer activities in melanoma cancers. Nevertheless, the compounds contain high antioxidant capacities and anticancer activities in melanoma cells, shown to be effective in hyperpigmentation disorders, but whether flavonoid glycosides from Z. jujuba regulate anti-melanogenesis remains unclear. In this study, we evaluated the anti-melanogenic activity of five flavonoid glycosides from Z. jujuba var. inermis (Bunge) Rehder seeds, including jujuboside A (JUA), jujuboside B (JUB), epiceanothic acid (EPA), betulin (BTL), and 6’’’-feruloylspinosin (FRS), in B16F10 melanoma cells and zebrafish larvae. According to our results, JUB, EPA, and FRS potently inhibited α-melanocyte-stimulating hormone (α-MSH)-induced melanogenesis and prevented hyperpigmentation in zebrafish larvae. In particular, under α-MSH-stimulated conditions, FRS most significantly inhibited α-MSH-induced intracellular and extracellular melanin content in B16F10 melanoma cells. Additionally, JUB, EPS, and FRS remarkably downregulated melanogenesis in α-MSH-treated zebrafish larvae, with no significant change in heart rate. Neither JUA nor BTA were effective in downregulating melanogenesis in B16F10 melanoma cells and zebrafish larvae. Furthermore, JUB, EPA, and FRS directly inhibited in vitro mushroom tyrosinase enzyme activity. JUB, EPA, and FRS also downregulated cyclic adenosine monophosphate (cAMP) levels and the phosphorylation of cAMP-response element-binding protein (CREB), and subsequent microphthalmia transcription factor (MITF) and tyrosinase expression. In conclusion, this study demonstrated that JUB, EPA, and FRS isolated from Z. jujuba var. inermis (Bunge) Rehder seeds exhibit potent anti-melanogenic properties by inhibition of the cAMP-CERB-MITF axis and consequent tyrosinase activity.

Fluvastatin increases tyrosinase synthesis induced by α-melanocyte-stimulating hormone in B16F10 melanoma cells

2010 ◽  
Vol 62 (1) ◽  
pp. 164-169 ◽  
Author(s):  
Ryszard Galus ◽  
Justyna Niderla ◽  
Dariusz Śladowski ◽  
Emir Sajjad ◽  
Krzysztof Włodarski ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
B16f10 Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Melanoma Cells ◽  
Stimulating Hormone

An In-Vitro Assay Estimating Changes in Melanin Content of Melanoma Cells due to Ultra-Dilute, Potentized Preparations

Homeopathy ◽  
2019 ◽  
Vol 108 (03) ◽  
pp. 183-187 ◽  
Author(s):  
Renuka Munshi ◽  
Samidha Joshi ◽  
Gitanjali Talele ◽  
Rajesh Shah
Keyword(s):  
In Vitro Study ◽  
Melanoma Cells ◽  
Tyrosinase Activity ◽  
Melanin Content ◽  
B16f10 Melanoma ◽  
Vitro Assay ◽  
Melanocyte Stimulating Hormone ◽  
B16f10 Melanoma Cells ◽  
Physiological Dose

Introduction The authors had previously conducted an in-vitro study to observe the effect of homeopathic medicines on melanogenesis, demonstrating anti-vitiligo potential by increasing the melanin content in murine B16F10 melanoma cells. A similar experiment was performed using further homeopathic preparations sourced from kojic acid (KA), hydrogen peroxide (H2O2; HP), 6-biopterin (BP), and [Nle4, D-Phe7]-α-melanocyte-stimulating hormone (NLE), some of which are known to induce vitiligo or melano-destruction at physiological dose. Materials and Methods The homeopathic preparations of BP, KA, NLE, and HP were used in 30c potency. Alcohol and potentized alcohol were used as vehicle controls. Prior to starting the main experiment, the viability of B16F10 melanoma cells after treatment with study preparations was assayed. Melanin content (at 48 h and 96 h) and tyrosinase activity in melanocytes were determined. Results At the end of 48 hours, NLE and HP in 30c potency had a significantly greater melanin content (p = 0.015 and p = 0.039, respectively) compared with controls; BP and KA in 30c potency had no significant effects. No significant changes were seen at the end of 96 hours. KA, NLE, HP, and vehicle controls showed an inhibition of tyrosinase activity. Conclusion The study demonstrated melanogenic effects of two homeopathic preparations. Further research to evaluate the therapeutic efficacy of these medicines is warranted.

scholarly journals Gamma-Aminobutyric Acid (GABA) Inhibits α-Melanocyte-Stimulating Hormone-Induced Melanogenesis through GABAA and GABAB Receptors

2021 ◽  
Vol 22 (15) ◽  
pp. 8257
Author(s):  
Ilandarage Menu Neelaka Molagoda ◽  
Mirissa Hewage Dumindu Kavinda ◽  
Hyung Won Ryu ◽  
Yung Hyun Choi ◽  
Jin-Woo Jeong ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Melanoma Cells ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
B16f10 Melanoma ◽  
Melanocyte Stimulating Hormone ◽  
Zebrafish Larvae ◽  
B16f10 Melanoma Cells ◽  
Gabaa And Gabab Receptors

Gamma-aminobutyric acid (GABA) is considered the primary inhibitory neurotransmitter in the human cortex. However, whether GABA regulates melanogenesis has not been comprehensively elucidated. In this study, we reveal that GABA (20 mM) significantly inhibited α-melanocyte-stimulating hormone (α-MSH)-induced extracellular (from 354.9% ± 28.4% to 126.5% ± 16.0%) and intracellular melanin contents (from 236.7% ± 11.1% to 102.7% ± 23.1%) in B16F10 melanoma cells, without inducing cytotoxicity. In addition, α-MSH-induced hyperpigmentation in zebrafish larvae was inhibited from 246.3% ± 5.4% to 116.3% ± 3.1% at 40 mM GABA, displaying no apparent cardiotoxicity. We also clarify that the GABA-mediated antimelanogenic properties were related to the direct inhibition of microphthalmia-associated transcription factor (MITF) and tyrosinase expression by inhibiting cyclic adenosine monophosphate (cAMP) and cAMP response element-binding protein (CREB). Furthermore, under α-MSH stimulation, GABA-related antimelanogenic effects were mediated through the GABAA and GABAB receptors, with subsequent inhibition of Ca2+ accumulation. In B16F10 melanoma cells and zebrafish larvae, pretreatment with bicuculline, a GABAA receptor antagonist, and CGP 46381, a GABAB receptor antagonist, reversed the antimelanogenic effect of GABA following α-MSH treatment by upregulating Ca2+ accumulation. In conclusion, our results indicate that GABA inhibits α-MSH-induced melanogenesis. Hence, in addition to the health benefits of GABA in the central nervous system, it could ameliorate hyperpigmentation disorders.

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