Pterosins from<i>Pteris multifida</i>

Ou-Yang, Dan-Wei; Ni, Xiang; Xu, Haiyan; Chen, Jia; Yang, Pei–Ming; Kong, Dandan

doi:10.1055/s-0030-1249934

Cited by 30 publications

(13 citation statements)

References 7 publications

(16 reference statements)

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“…Pterosin C and other C 14 and C 15 sesquiterpenoids, along with C 20 -monoxygenated ent-kaurane diterpenoids and 4, 5-dicaffeoylquinic acid, were identified as the cytotoxic constituents of P. multifida Poir. (Ge et al 2008;Harinantenaina et al 2008;Ouyang et al 2010). The pterosin sesquiterpenes 2R,3R-13-hydroxypterosin L 3-O-D-glucopyranoside, 2R,3S-acetylpterosin C, and 2S,3S-acetylpterosin C also showed cytotoxicity against HL 60 cells with IC 50 values of 14.6, 48.3 and 35.7 mM, respectively (Shu et al 2012).…”

Section: Anticancer Activitymentioning

confidence: 99%

Phytochemicals from fern species: potential for medicine applications

et al. 2017

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Ferns are an important phytogenetic bridge between lower and higher plants. Historically they have been used in many ways by humans, including as ornamental plants, domestic utensils, foods, and in handicrafts. In addition, they have found uses as medicinal herbs. Ferns produce a wide array of secondary metabolites endowed with different bioactivities that could potentially be useful in the treatment of many diseases. However, there is currently relatively little information in the literature on the phytochemicals present in ferns and their pharmacological applications, and the most recent review of the literature on the occurrence, chemotaxonomy and physiological activity of fern secondary metabolites was published over 20 years ago, by Soeder (Bot Rev 51:442–536, 1985). Here, we provide an updated review of this field, covering recent findings concerning the bioactive phytochemicals and pharmacology of fern species

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Section: Anticancer Activitymentioning

confidence: 99%

Phytochemicals from fern species: potential for medicine applications

et al. 2017

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“…Seven phase I metabolites are known and were identified as (2R,3S)-pterosin L (M1) Kuroyanagi et al, 1979a) (Fukuoka et al, 1972(Fukuoka et al, , 1983Kuroyanagi et al, 1979a), (2R,3 S)-pterosin C (M6), (2S,3S)-pterosin C (M8) , (Ϯ)-pterosin P (M10) (Kuroyanagi et al, 1979b;Ouyang et al, 2010), (Ϯ)-pterosin E (M18) (Yoshihira et al, 1971), and (Ϯ)-pterosin B (M19) (Yoshihira et al, 1971;Sengupta et al, 1976), respectively, by comparison of their spectroscopic data (MS, 1 H, 13 C NMR, NOEDS, and CD) ( Table 1; Supplemental Tables S1 and S2) with those reported in the literatures. Of these, M10, M18, and M19 were obtained as racemic form deduced from the transparent CD spectra.…”

Section: (2s)-pterosin a Metabolites In Rat Urinementioning

confidence: 99%

“…at ASPET Journals on May 11, 2018 dmd.aspetjournals.org Downloaded from possessed much weaker cytotoxicity Ouyang et al, 2010). Nevertheless, M8 could enhance glucose consumption and the expression of glucose transporter 4 (Hsu et al, 2010) and thus could be considered as an active metabolite.…”

Section: (2s)-pterosin a Metabolites In Rat Urinementioning

confidence: 99%

Metabolism of (2S)-Pterosin A: Identification of the Phase I and Phase II Metabolites in Rat Urine

Lee¹,

Hsu²,

Kang³

et al. 2012

Drug Metab Dispos

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ABSTRACT:The metabolic profile of the potent hypoglycemic agent, (2S)-pterosin A (1), in rat urine via intragastrical oral administration was investigated. In total, 19 metabolites (M1-M19) were identified. Among these, 16 metabolites were characterized by high-performance liquid chromatography solid-phase extraction-tube transfer-NMR, and seven metabolites were further isolated from the treated urine to enable further structural determination. Twelve of these are new compounds. The phase I metabolites of 1 were formed via various oxidations at positions C-3, C-10, C-12, C-13, or C-1 followed by decarboxylation of C-10 or C-14, and lactonization at C-12/C-14 or C-14/C-12. The phase II metabolites were glucuronide conjugates from the parent compound or phase I metabolites. The major metabolites were found to be (2S)-14-O-glucuronylpterosin A (M9), (2S)-2-hydroxymethylpterosin E (M14), and (؎)-pterosin B (M19). Quantitative HPLC analysis of metabolites, based on similar UV absorption and use of the regression equation of 1, indicated that ϳ71% 1 was excreted as metabolites in rat urine.

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“…Several fern plants have been shown to possess hypolipidemic, hypoglycemic, vascular protective, anti-inflammatory, and antinociceptive activities (9–12). Several pterosin compounds isolated from fern plants have been shown to have smooth muscle relaxant, leishmanicidal, and anticancer activities in vitro (13–15). The antidiabetic activity of pterosin compounds still remains unclear.…”

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confidence: 99%

Antidiabetic Effects of Pterosin A, a Small-Molecular-Weight Natural Product, on Diabetic Mouse Models

et al. 2013

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The therapeutic effect of pterosin A, a small-molecular-weight natural product, on diabetes was investigated. Pterosin A, administered orally for 4 weeks, effectively improved hyperglycemia and glucose intolerance in streptozotocin, high-fat diet–fed, and db/db diabetic mice. There were no adverse effects in normal or diabetic mice treated with pterosin A for 4 weeks. Pterosin A significantly reversed the increased serum insulin and insulin resistance (IR) in dexamethasone-IR mice and in db/db mice. Pterosin A significantly reversed the reduced muscle GLUT-4 translocation and the increased liver phosphoenolpyruvate carboxyl kinase (PEPCK) expression in diabetic mice. Pterosin A also significantly reversed the decreased phosphorylations of AMP-activated protein kinase (AMPK) and Akt in muscles of diabetic mice. The decreased AMPK phosphorylation and increased p38 phosphorylation in livers of db/db mice were effectively reversed by pterosin A. Pterosin A enhanced glucose uptake and AMPK phosphorylation in cultured human muscle cells. In cultured liver cells, pterosin A inhibited inducer-enhanced PEPCK expression, triggered the phosphorylations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase phosphorylation, and increased the intracellular glycogen level. These findings indicate that pterosin A may be a potential therapeutic option for diabetes.

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Pterosins fromPteris multifida

Cited by 30 publications

References 7 publications

Phytochemicals from fern species: potential for medicine applications

Phytochemicals from fern species: potential for medicine applications

Metabolism of (2S)-Pterosin A: Identification of the Phase I and Phase II Metabolites in Rat Urine

Antidiabetic Effects of Pterosin A, a Small-Molecular-Weight Natural Product, on Diabetic Mouse Models

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