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Insulin resistance has become a worldwide nutrition and metabolic health problem due to the lack of effective protective agents. Laminaria japonica is a well-known marine vegetable. Purified Laminaria japonica polysaccharide (LJP61A) can inhibit atherosclerosis in high-fat-diet (HFD)-fed mice via ameliorating insulin resistance. In this study, we aimed to clarify the mechanism by which LJP61A ameliorates HFD-induced insulin resistance. The results indicated that HFD-induced insulin resistance, obesity, systematic inflammation, metabolic endotoxemia, and gut permeability in mice could be reduced by LJP61A. Gut microbiota analysis showed that the gut microbiota dysbiosis of HFD-fed mice, especially the reduction in mucin-degrading Akkermansia, could be reversed by LJP61A. Additionally, the reduction in mucin-producing goblet cells in HFD-fed mice could also be reversed by LJP61A. Moreover, insulin resistance, obesity, systematic inflammation, metabolic endotoxemia, and gut microbiota dysbiosis in HFD-fed mice could also be alleviated by faecal transplant from LJP61A-treated mice. Overall, LJP61A might be used as a prebiotic to ameliorate HFD-induced insulin resistance and associated metabolic disorders via regulating gut microbiota, especially Akkermansia.

The present work aims to investigate the effects and underlying mechanism of a homogeneous Laminaria japonica polysaccharide (LJP61A) on acute kidney injury (AKI) in mice. According to the results of biochemical and pathological analysis, we concluded that LJP61A could protect kidney from the damage of adriamycin in AKI mice. Compared to the model group, the mRNA level of cytokines (TNF-α, IL-1β and MCP-1) and protein level of mesenchymal markers demsin were decrease by the treatment of LJP61A while the protein levels of podocyte structure markers (Nephrin and WT-1) were increased. Moreover, the adriamycin-induced enhancement of phosphor-p65, phosphor-p38, phosphor-ERK1/2 and phosphor-JNK in the kidney of AKI mice were significantly suppressed by LJP61A. Similar variation was observed in the mRNA and protein levels of TGF-β1 and Smad3. These results suggested that LJP61A prevented acute kidney injury possibly via regulating TGF-β1-mediated Smad3, MAPKs and NF-κB signaling pathways.

Promoting M1 polarization of tumor-associated macrophages (TAMs) is an effective pathway for malignant tumor therapy. In this study, we aimed to demonstrate whether homogeneous Dendrobium officinale polysaccharide (DOP) could promote M1 polarization of TAMs to inhibit tumor growth, and how it promoted. Results exhibited that DOP could inhibit the tumor growth and promote the M1 polarization of TAMs in tumor-bearing mice. Macrophage depletion and replenishment experiment clearly proved that the inhibitory effect of DOP on tumor growth is dependent on promoting M1 polarization of TAMs. Moreover, we found that DOP could reach tumor microenvironment (TME) and directly bind to TAMs to promote its M1 polarization via targeting toll-like receptor 2 (TLR2) after oral administration. These results clarified that DOP could remarkably inhibit the tumor growth of tumor-bearing mice via directly targeting the TLR2 of TAMs to promote its M1 polarization.

Parkinson's disease (PD) is an age-related neurodegenerative disorder without effective treatments. Mesencephalic astrocyte-derived neurotrophic factor (MANF) has been suggested to be capable of protecting against PD by inhibiting endoplasmic reticulum (ER) stress-mediated neuronal apoptosis.This study was aimed to evaluate the antiparkinsonian effect of dendrobine and reveal its underlying mechanisms from the perspective of MANF-mediated ER stress suppression.Behavioral assessments of PD mice as well as LDH/CCK-8 assay in SH-SY5Y cells and primary midbrain neurons were carried out to detect the antiparkinsonian effect of dendrobine. Immunofluorescence, western blot, flow cytometry and shRNA-mediated MANF knockdown were used to determine the apoptosis of dopaminergic neurons and the expressions of ER stress-related proteins for investigating the underlying mechanism of dendrobine.Dendrobine significantly ameliorated the motor performance of PD mice and attenuated the injuries of dopaminergic neurons. Dendrobine could also relieve neuronal apoptosis, up-regulate MANF expression and inhibit ER stress, which were largely abolished by shRNA-mediated MANF knockdown in PD model.Dendrobine might protect against PD by inhibiting dopaminergic neuron apoptosis, which was achieved by facilitating MANF-mediated ER stress suppression. Our study suggested that dendrobine could act as a MANF up-regulator to protect against PD, and provided a potential candidate for exploring etiological agents of PD.

A new polysaccharide (cDFP-W1) with high immunostimulatory activities was isolated from the stems of Dendrobium fimbriatum Hook. The analysis of the physicochemical properties showed that cDFP-W1 consisted of mannose and glucose in a molar ratio of 1 : 3.84, and its relative molecular weight was 4.0 × 104 Da. Structural analysis implied that the linear backbone of cDFP-W1 was composed of α-1,4-D-Glcp, β-1,4-D-Manp, 3-O-acetyl-α-1,4-D-Glcp and α-1,4,6-D-Glcp, and its branches were the terminal β-D-Manp that was attached to the C-6 position of α-1,4,6-D-Glcp. An in vivo immunostimulatory assay exhibited that cDFP-W1 at 200 mg kg−1 could significantly increase the proportions of CD4+ T-cell subpopulations, B cells, natural killer cells and dendritic cells, decrease the proportion of CD8+ T-cell subpopulations, and upregulate the percentage of activated macrophages (p < 0.01) in the spleen of mice. An in vitro immunostimulatory assay revealed that cDFP-W1 could effectively promote the proliferation of spleen lymphocytes, enhance the proliferation and phagocytosis of macrophage RAW264.7 cells, and stimulate the mRNA expression and extracellular release of NO, TNF-α and IL-1β of RAW264.7 cells. The western blot experiment suggested that the immunostimulatory activities of cDFP-W1 were closely related to the activation of MAPKs, NF-κB and PI3K/Akt signaling pathways.

With fluorescent end-labeling method, a homogenous Dendrobium huoshanense polysaccharide (GXG) that was orally administrated to mice was found to be degraded into a stable fragment (dGXG) in the stomach, where dGXG was propelled into the small intestine and absorbed into the systemic circulation. The residual GXG in the stomach could pass through the gastrointestinal tract and was excreted into faeces with a very slow fermentation in the large intestine. The simulated digestion of GXG indicated that the acidic pH condition in the gastric fluid was responsible for GXG degradation, which was supported by the oral digestion of dGXG. Chemical analysis not only showed a change in the molar ratio of monosaccharide compositions and glycosidic linkage types, but also found the loss of the sugar residue (1→4)-linked Galp after the acid treatment of GXG, suggesting that the cleavage of glycosidic linkage, especially (1→4)-linked Galp linkage, resulted in GXG degradation in the gastrointestinal tract.

In this work, we investigated the effect of Chinese chive polysaccharides (CCP) on renal function in mice with adenine-induced chronic renal failure (CRF). Results exhibited that adenine treatment caused serious renal pathological damages and elevation of serum creatinine and blood urea nitrogen of mice. However, these changes could be significantly reversed by the administration of CCP in a dose-dependent manner. When CCP dosage reached 200mg/kg/day, the area of renal pathological damage was decreased by 59.2%, and the levels of serum creatinine and blood urea nitrogen were decreased by 23.9% and 34.7% compared to those of model group. Moreover, it was found that renal oxidative damage, inflammation and fibrosis of adenine-induced CRF mice could also be significantly inhibited by CCP. These results suggested that CCP could improve the kidney functions of adenine-induced CRF mice and the renoprotective effect might be associated with its antioxidant, anti-inflammatory and anti-fibrosis activities.

A new polysaccharide (JSP-11) with a molecular weight of 1.25 × 106 Da was extracted and purified from jellyfish. Monosaccharide analysis showed that JSP-11 was composed of mannose, galactose and glucuronic acid with a molar ratio of 2.18:1.00:1.94. According to the analysis of fourier transform-infrared spectroscopy, methylation analysis, and NMR spectroscopy, JSP-11 was determined to contain a linear backbone which consisted of (1 → 3,6)-linked β- d -Manp and (1 → 6)-linked β- d -Galp. The branch of (1→)-linked α- d -GlcpA was attached to the C-3 position of (1 → 3,6)-linked β- d -Manp in the backbone. The immunomodulatory assay exhibited that JSP-11 could significantly enhance the viability of RAW 264.7 macrophage cells, and promote the release of NO, TNF-α, and IL-1β via activating NF-κB, MAPKs and PI3K/Akt signal pathways.

In this study, whey protein isolate (WPI)-quercetin (Que)-lotus root amylopectin (LRA) hydrogels (WPI-QUE-LRA) was developed to improve the solubility, stability and bioavailability of quercetin. Results showed that the favorable WPI-QUE-LRA was formed using WPI and LRA in the ratio of 1:2 at pH 7.0. Under this condition, the average size, polydispersity index, zeta potential of the WPI-QUE-LRA was 179.5 nm, 0.271, -18.6 mV, respectively. The analysis of transmission electron microscopy, fourier transform infrared spectroscopy and X-ray diffractometer revealed that the quercetin was successfully encapsulated in WPI-LRA, giving a high encapsulation efficiency of 92.4 %. Moreover, the WPI-LRA could significantly improve the storage stability and photochemical stability of quercetin. The in vitro and in vivo experiments showed that LRA-coated WPI hydrogel can enable quercetin to be stable in stomach and be effectively released in small intestine, leading to the enhancement of the bioavailability of quercetin.

The structure features and anti-gastric cancer activities in vitro of stem, root, leaf and flower polysaccharides from cultivated Dendrobium huoshanense were investigated systematically. Stem polysaccharide (cDHPS) was composed of →4)-β-D-Glcp-(1→, →4)-β-D-Manp-(1→, →4)-3-O-acetyl-β-D-Manp-(1→ with the molecular weight of 2.59 × 105 Da; root polysaccharide (cDHPR) was composed of →3,5)-α-L-Araf-(1→, →4)-β-D-Glcp-(1→, →4)-β-D-Manp-(1→, →4,6)-β-D-Manp-(1→, →6)-α-D-Galp-(1→ and terminal β-L-Araf with the molecular weight of 1.41 × 104 Da; leaf polysaccharide (cDHPL) was composed of →4)-β-D-Glcp-(1→, →4)-β-D-Manp-(1→, →4)-3-O-acetyl-β-D-Manp-(1→, →3,6)-β-D-Manp-(1→ and terminal α-D-Galp with the molecular weight of 2.09 × 105 Da; and flower polysaccharide (cDHPF) was composed of →4)-β-D-Glcp-(1→, →4)-β-D-Manp-(1→, →3,6)-β-D-Manp-(1→ and terminal α-D-Galp with the molecular weight of 4.78 × 105 Da. Among these four polysaccharides, cDHPS showed the best anti-gastric cancer activity evidenced by the inhibited growth and c-myc expression as well as the enhanced apoptosis and p53 expression of murine forestomach carcinoma (MFC) cells, suggesting their difference in anti-gastric cancer activity should be contributed to their difference in structure features.

Chronic renal failure (CRF) is a major public health problem worldwide. In this work, we investigated the effects of a purified Laminaria japonica polysaccharide (LJP61A) on renal function using an adenine-induced CRF mice model. Results exhibited that adenine treatment caused serious renal pathological damages and elevation of serum creatinine and blood urea nitrogen of mice. However, these changes could be significantly reversed by the administration of LJP61A in a dose-dependent manner. Additionally, LJP61A could dramatically reduce weight loss, improve the urine biochemical index, and regulate the electrolyte disturbance of CRF mice. These results suggest that the renal function of adenine-induced CRF mice can be improved by LJP61A, which might be developed into a potential therapeutic agent for CRF patients.

The present study explored the beneficial effect of Dendrobium huoshanense stem polysaccharide (cDHPS) after oral administration on rheumatoid arthritis (RA) using type Ⅱ collagen-induced arthritis (CIA) mouse model. It was found that cDHPS effectively alleviated joint swelling, synovial hyperplasia, pannus formation, cartilage erosion and bone destruction in CIA mice. Concurrently, cDHPS remodeled the balance of Th17 and regulatory T cells, reduced the secretion of pro-inflammatory mediators related to fibroblast-like synoviocyte activation, angiogenesis, articular cartilage degradation and osteoclast differentiation, inhibited HIF-1α expression and promoted anti-inflammatory mediator release in the joint tissues and serum of CIA mice. Western blot of joint tissues showed that cDHPS significantly inhibited the phosphorylation of IκB, p65, JNK, p38, ERK1/2, AKT, PI3K, JAK1 and STAT3 in CIA mice. These results suggest that cDHPS possesses the potential of ameliorating RA and its anti-RA effect may be attributed to the inhibition of inflammatory signaling pathways.

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This study aimed to investigate the effect and underlying mechanism of a purified Laminaria japonica polysaccharide (LJP61A) on preventing vascular calcification (VC). In the adenine-induced chronic renal failure (CRF) mice VC model and the β-glycerophosphate (β-GP)-induced vascular smooth muscle cells (VSMC) calcification model, LJP61A was found to significantly inhibit VC phenotypes as determined by biochemical analysis and von Kossa, alizarin red, and immunohistochemical staining. Meanwhile, LJP61A remarkably up-regulated the mRNA levels of VSMC related markers and down-regulated the mRNA levels of sodium-dependent phosphate cotransporter Pit-1. In addition, LJP61A could significantly decrease the protein levels of core-binding factor-1, osteocalcin, bone morphogenetic protein 2, and receptor activator for nuclear factor-κB ligand, and it can increase the protein levels of osteoprotegerin and matrix gla protein. These results indicated that LJP61A ameliorated VC both in vivo and in vitro via preventing osteoblastic differentiation of VSMC, suggesting LJP61A might be a potential therapeutic agent for VC in CRF patients.

In this work, a purified Laminaria japonica polysaccharide (LJP61A) was chemically modified to obtain three sulfated polysaccharides (SLJP1, SLJP2 and SLJP3) with different degrees of sulfation using the method of chlorosulfonic acid/pyridine. The effects and underlying mechanism of SLJP1, SLJP2 and SLJP3 on the suppression of macrophage foam cell formation were further investigated using the model of oxidized low-density lipoprotein (ox-LDL)-induced foam cell formation. Results exhibited that the macrophage foam cell formation induced by ox-LDL could be significantly alleviated by these sulfated polysaccharides in a dose-dependent manner. Meanwhile, the enhancement of PPAR-γ mRNA expression in ox-LDL induced macrophages was remarkably inhibited by these sulfated polysaccharides. Moreover, the cellular inflammation induced by ox-LDL could also be remarkably mitigated by these sulfated polysaccharides. These results indicated that the sulfated L. japonica polysaccharides could inhibit the conversion of macrophage into foam cell via obstructing PPAR-γ activation and alleviating cellular inflammation.

High concentrations of arsenic, which can be occasionally found in drinking water, have been recognized as a global health problem. Exposure to arsenic can disrupt spatial memory; however, the underlying mechanism remains unclear. In the present study, we tested whether exercise could interfere with the effect of arsenic exposure on the long-term memory (LTM) of object recognition in mice. Arsenic (0, 1, 3, and 10 mg/ kg, i.g.) was administered daily for 12 weeks. We found that arsenic at dosages of 1, 3, and 10 mg/kg decreased body weight and increased the arsenic content in the brain. The object recognition LTM (tested 24 h after training) was disrupted by 3 mg/ kg and 10 mg/ kg, but not 1 mg/ kg arsenic exposure. Swimming exercise also prevented LTM impairment induced by 3 mg/ kg, but not with 10 mg/ kg, of arsenic exposure. The expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP-response element binding protein (pCREB) in the CA1 and dentate gyrus areas (DG) of the dorsal hippocampus were decreased by 3 mg/ kg and 10 mg/ kg, but not by 1 mg/ kg, of arsenic exposure. The decrease in BDNF and pCREB in the CA1 and DG induced by 3 mg/ kg, but not 10 mg/ kg, of arsenic exposure were prevented by swimming exercise. Arsenic exposure did not affect the total CREB expression in the CA1 or DG. Taken together, these results indicated that swimming exercise prevented the impairment of object recognition LTM induced by arsenic exposure, which may be mediated by BDNF and CREB in the dorsal hippocampus.

A new sesquiterpenoid, 1, and three new diterpenoids, 3-5, along with five known compounds, 2 and 6-9, were isolated from rhizomes of Alpinia japonica. The structures of the new compounds were determined as (1R,4R,6S,7S,9S)-4α-hydroxy-1,9-peroxybisabola-2,10-diene (1), methyl (12E)-16-oxolabda-8(17),12-dien-15-oate (3), (12R)-15-ethoxy-12-hydroxylabda-8(17),13(14)-dien-16,15-olide (4), and methyl (11E)-14,15,16-trinorlabda-8(17),11-dien-13-oate (5) by means of spectroscopic data. The absolute configurations at C(4) in 1 and C(12) in 4 were deduced from the circular dichroism (CD) data of the in situ-formed [Rh2 (CF3 COO)4 ] complexes. Inhibitory effects of the isolates on NO production in lipopolysaccharide-induced RAW264.7 macrophages were evaluated, and 2-4, 6, and 7 were found to exhibit inhibitory activities with IC50 values between 14.6 and 34.3 μM.

A novel norsesquiterpene ( 1 ), three new bisabolenes sesquiterpenes ( 2 – 4 ), along with 7 known compounds ( 5 – 11 ), were isolated from the rhizomes of Alpinia japonica . The structures of the new compounds were elucidated by analysis of spectroscopic data. The absolute configuration of C-1 in 3 was deduced via the circular dichroism data of the in situ formed [Rh 2 (OCOCF 3 ) 4 ] complexes. Inhibitory effects of the isolates on nitric oxide production in lipopolysaccaride-activated RAW264.7 macrophages were evaluated. Compound 6 showed significant inhibitory activity with IC 50 value of 5.3 μΜ, and compounds 1 , 3 , 5 and 7 – 10 exhibited moderate inhibitory activities with IC 50 values between 24.5 and 46.3 μM.