dicliptera sexangularis/polysaccharide

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Hepatoprotective effects of Dicliptera chinensis polysaccharides on dimethylnitrosamine-induced hepatic fibrosis rats and its underlying mechanism.

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BACKGROUND Dicliptera chinensis is a traditional herbal medicine used anciently in China for hepatopathy treatment, especially in south areas. Our several studies have demonstrated that dicliptera chinensis polysaccharides (DCP), which has a markedly protective effects on chemistry-induced models of

Isolation, characterization and bioactivities of the polysaccharides from Dicliptera chinensis (L.) Juss.

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The polysaccharides of Dicliptera chinensis (L.) Juss. (DCP-1 and DCP-2) were extracted and isolated using the methods of water extract-ethanol precipitate and sephadex column chromatography and characterized by gel permeation chromatography (GPC), Fourier transform infrared spectrometry (FT-IR) and

Polysaccharides from Dicliptera chinensis ameliorate liver disturbance by regulating TLR-4/NF-κB and AMPK/Nrf2 signalling pathways.

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The purpose of this study was to alleviate liver disturbance by applying polysaccharides from Dicliptera chinensis (DCP) to act on the adenosine monophosphate-activated protein kinase/ nuclear factor erythroid 2-related factor 2 (AMPK/ Nrf2) oxidative stress pathway and the Toll-like receptor 4

[Studies on structure characteristic of polysaccharide P1A from Dicliptera chinensis].

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The chemical structures of P1 A was identified by complete acid hydrolysis, partial acid hydrolysis, periodate oxidation-Smith degradation, methylation analysis, IR and NMR. The results showed that P1 A had a backbone consisting rhamnose, mannose, glucose and galactose. The side chain possessed

Dicliptera Chinensis polysaccharides target TGF-β/Smad pathway and inhibit stellate cells activation in rats with dimethylnitrosamine-induced hepatic fibrosis.

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This study aims to study impact of Dicliptera chinensis polysaccharide (DCP) on hepatic fibrosis (HF) and activation of hepatic stellate cells (HSCs). Liver fibrosis model was induced by intraperitoneal injection of dimethyl nitrosamines (DMN) in rat. Rats in treatment group were administrated with

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