Natural Products Chemistry & Research

ISSN - 2329-6836


Anti-Adipogenic Polyphenols of Water Shield Suppress TNF-α-Induced Cell Damage and Enhance Expression of HAS2 and HAPB2 in Adiponectin-Treated Dermal Fibroblasts

Hiroshi Shimoda, Seikou Nakamura, Shoketsu Hitoe, Shuko Terazawa, Junji Tanaka, Takahiro Matsumoto and Hisashi Matsuda

Water shield (Brasenia schreberi J. F. Gmel) is an aquatic plant cultivated in Northern Japan, from which we have isolated polyphenolic compounds including a novel flavonol glycoside, junsainoside A. Recently, dermal fibroblasts have reported to be affected by adipocytokines from subcutaneous adipocytes. Hence, we evaluated the effects of polyphenolic compounds from water shield on fat accumulation, adipocytokine release and adipocytokine-induced fibroblast status. In differentiated 3T3-L1 adipocytes, ethyl gallate, caffeoyl glucose, hypolaetin 7-O-glucoside, kaempferol and junsainoside A significantly suppressed lipid accumulation at 10 μM. In addition to these constituents, ferulic acid, kaempferol 3-O-(6"-galloyl) glucoside, quercetin 3-O-(6"-galloyl) glucoside, quercetin 3-O-glucoside and gossypetin suppressed the lipid accumulation in human subcutaneous adipocytes. Ethyl gallate and junsainoside A also enhanced adiponectin production from subcutaneous adipocytes without induction of TNF-α release. On the other hand, ethyl gallate and quercetin recovered from TNF- α-induced fibroblast damage. Moreover, ferulic acid, quercetin and kaempferol enhanced the expression of hyaluronan binding protein 2 and hyaluronan synthase 2 in adiponectintreated fibroblasts. These results suggested that water shield contains various types of polyphenolic compounds with anti-adipogenic activity, some of which protect dermal fibroblasts from TNF-α damage and probably enhance hyaluronan production. It is assumed that polyphenols in water shield maybe suppress subcutaneous fat accumulation and maintain dermal fibroblast and hyaluronan-related status.