Structural characterization and immunomodulatory activity of an arabinogalactan from Jasminum sambac (L.) Aiton tea processing waste.

An arabinogalactan named JSP-1a was isolated from Jasmine tea processing waste by DEAE Sepharose FF and Sephacryl S-200 HR chromatography. Polysaccharide JSP-1a, with an average molecular weight of 87.5 kDa, was composed of galactose (59.60 %), arabinose (33.89 %), mannose (4.81 %), and rhamnose (1.70 %). JSP-1a was found to be a type II arabinogalactan comprising the main backbone of 1, 6-linked Galp residues, and the side chain containing α-T-Araf, α-1,5-Araf, ß-T-Galp, ß-1,3-Galp, and ß-1,4-Manp residues was attached to the O-3 position of ß-1,3,6-Galp residues. Evidence from bioactivity assays indicated that JSP-1a possessed potent immunomodulatory effects on RAW264.7 macrophages: treatment with JSP-1a increased phagocytosis, activated NF-κB p65 translocation, and promoted the production of NO, reactive oxygen species (ROS), the tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Furthermore, inhibition of Toll-like receptor 4 caused the suppression of NO release and cytokines secretion, which indicated that TLR-4/NF-κB pathway might play a significant role in JSP-1a-induced macrophages' immune response. The results of this study could provide a theoretical basis of JSP-1a as a safe immunostimulatory functional foods or a treatment for immunological diseases.

Structure characteristics, hypoglycemic and immunomodulatory activities of pectic polysaccharides from Rosa setate x Rosa rugosa waste.

In this study, two polysaccharide components named WSRP-2a and WSRP-2b, were purified from Rosa setate x Rosa rugosa waste via anion exchange and gel filtration chromatography. Monosaccharide composition, Congo red assay, FT-IR and NMR spectra analysis confirmed that both of these fractions were mainly composed of galacturonic acid, arabinose, galactose and rhamnose, which were pectin-type polysaccharides with non-triple-helix structure. WSRP-2a and WSRP-2b, however, differed in molecular weight of 56.8 kD and 23.9 kD. The followed bioassay presented their impressive hypoglycemic and immunomodulatory activities. WSRP-2a promoted more proliferation, NO release, and the secretion of cytokines in RAW264.7 macrophages, while WSRP-2b presented higher α-amylase and α-glucosidase inhibitory activities. Collectively, these results suggested that the Rosa Setate x Rosa Rugosa waste biomass could be used as a promising source of bioactive pectic polysaccharides.

Chicoric acid suppresses BAFF expression in B lymphocytes by inhibiting NF-κB activity.

B cell activating factor belonging to the TNF family (BAFF) plays a critical role in the pathogenesis of autoimmune diseases. The inhibition of BAFF expression is an emerging therapeutic approach for these disorders. Chicoric acid (CA), a bioactive phytochemical found in several widely used traditional medicinal plants, has significant anti-inflammatory activity and anti-arthritic effects. However, the role of CA in modulation of BAFF expression remains unknown. In this study, we demonstrated that CA reduced BAFF expression in human B lymphocyte cell lines and decreased the DNA-binding activity of nuclear factor-κB (NF-κB) in the BAFF promoter region. Furthermore, CA inhibited both the nuclear translocation of p65 (the subunit of NF-κB) and the phosphorylation of IκBα (inhibitor of NF-κB). These results suggest that CA suppresses BAFF expression by inhibiting NF-κB activity, and CA may serve as a novel therapeutic agent to down-regulate excessive BAFF expression in autoimmune diseases.

Panax notoginseng saponins attenuate atherosclerosis via reciprocal regulation of lipid metabolism and inflammation by inducing liver X receptor alpha expression.

ETHNOPHARMACOLOGICAL RELEVANCE: Panax notoginseng (Burk.) F.H. Chen has been used as a health product and natural remedy in traditional medicine for cardiovascular diseases for more than 1000 years in Asia, including China, Japan, and Korea. Panax notoginseng saponins (PNS) are the major effective ingredients extracted from Panax notoginseng. AIM OF THE STUDY: The purpose of this study was to investigate whether Panax notoginseng saponins (PNS) attenuated atherosclerosis by inducing liver X receptor alpha (LXRα) expression and to elucidate the mechanisms responsible for the effects. MATERIALS AND METHODS: The AS rats were treated once daily with PNS (100 mg/kg, i.p.), and pathological changes in the aorta were observed using Sudan IV staining. The expression of LXRα in the aortic wall was measured by Western blot analysis. THP-1 macrophages were cultured with PNS in the presence or absence of geranylgeranyl pyrophosphate ammonium salt (GGPP), an LXRα antagonist. The expression of LXRα and its target genes ATP-binding cassette A1 and G1 (ABCA1, ABCG1) were determined by qRT-PCR. The transcriptional activation of the LXRα gene promoter was analyzed by a reporter assay. The NF-κB DNA binding activity and the expression of interleukin (IL)-6, monocyte chemotactic protein-1 (MCP-1) was evaluated respectively by Trans-AM NF-κB ELISA and ELISA in THP-1 macrophages that were stimulated with LPS after treatment with PNS and GGPP. RESULTS: PNS treatment alleviated the typical pathological changes associated with atherosclerosis in rats. The expression of LXRα was increased in rat aortas after treatment with PNS. In vitro, PNS increased LXRα mRNA levels in THP-1 macrophages. The reporter assays showed that PNS enhanced transcriptional activation of the LXRα gene promoter and led to the upregulation of ABCA1 and ABCG1 expression. This upregulation could be reversed by treatment with GGPP. Additionally, PNS inhibited NF-κB DNA binding activity and reduced secretion of IL-6 and MCP-1 in LPS-stimulated THP-1 macrophages. These effects could be reversed by GGPP. CONCLUSIONS: The results indicated that the PNS-mediated attenuation of AS may, at least partly, due to LXRα uprergulation. The mechanisms of action included enhancement transcriptional activation of the LXRα gene promoter by PNS and subsequent upregulation of ABCA1 and ABCG1 and inhibition of NF-κB DNA binding activity.