Anti-Melanogenesis Effects of Lotus Seedpod In Vitro and In Vivo.

Jen-Ying Hsu,Ting-Shuan Li,Jing-Hsien Chen,Yueching Wong,Chaio-Yun Tseng,Hui-Hsuan Lin

doi:10.3390/nu12113535

Jen-Ying Hsu, Ting-Shuan Li + Show 4 more

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https://doi.org/10.3390/nu12113535

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Abstract

Melanogenesis has many important physiological functions. However, abnormal melanin production causes various pigmentation disorders. Melanin synthesis is stimulated by α-melanocyte stimulating hormone (α-MSH) and ultraviolet (UV) irradiation. Lotus seedpod extract (LSE) has been reported as possessing antioxidative, anti-aging, and anticancer activities. The present study examined the effect of LSE on melanogenesis and the involved signaling pathways in vitro and in vivo. Results showed that non-cytotoxic doses of LSE and its main component epigallocatechin (EGC) reduced both tyrosinase activity and melanin production in the α-MSH-induced melanoma cells. Western blotting data revealed that LSE and EGC inhibited expressions of tyrosinase and tyrosinase-related protein 1 (TRP-1). Phosphorylation of p38 and protein kinase A (PKA) stimulated by α-MSH was efficiently blocked by LSE treatment. Furthermore, LSE suppressed the nuclear level of cAMP-response element binding protein (CREB) and disturbed the activation of melanocyte inducing transcription factor (MITF) in the α-MSH-stimulated B16F0 cells. The in vivo study revealed that LSE inhibited melanin production in the ear skin of C57BL/6 mice after exposure to UVB. These findings suggested that the anti-melanogenesis of LSE involved both PKA and p38 signaling pathways. LSE is a potent novo natural depigmenting agent for cosmetics or pharmaceutical applications.

Highlights

Melanin produced by melanocytes through melanogenesis directly affects the color of skin, hair, and eyes
The major extrinsic factor of melanogenesis is UV radiation acting through the melanocortin-1 receptor (MC1R) that is activated by α-melanocyte-stimulating hormone (α-MSH) [2]
10, 15, and 20 μg/mL Lotus seedpod extract (LSE) and 15 μM EGC (Figure 4c, lanes 3 to 6). These results indicated that LSE and EGC interfered with the cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB) and melanocyte inducing transcription factor (MITF) binding to their promoters to regulate tyrosinase and Tyrp1 gene expressions

Summary

Introduction

Melanin produced by melanocytes through melanogenesis directly affects the color of skin, hair, and eyes. Melanin protects the skin from ultraviolet (UV) stimulation. Abnormal melanogenesis causes hypo- or hyper-pigmentation disease and impacts the patient’s quality of life. Melanogenesis is influenced by intrinsic and extrinsic factors. Intrinsic factors of melanogenesis are resulted from overproduction of second messenger cyclic adenosine monophosphate (cAMP) which might occur during pregnancy and inflammation [1]. The major extrinsic factor of melanogenesis is UV radiation acting through the melanocortin-1 receptor (MC1R) that is activated by α-melanocyte-stimulating hormone (α-MSH) [2]

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