Tea Polysaccharide Ameliorates High-Fat Diet-Induced Renal Tubular Ectopic Lipid Deposition via Regulating the Dynamic Balance of Lipogenesis and Lipolysis.

Renal tubular ectopic lipid deposition (ELD) plays a significant role in the development of chronic kidney disease, posing a great threat to human health. The present work aimed to explore the intervention effect and potential molecular mechanism of a purified tea polysaccharide (TPS3A) on renal tubular ELD. The results demonstrated that TPS3A effectively improved kidney function and slowed the progression of tubulointerstitial fibrosis in high-fat-diet (HFD)-exposed ApoE-/- mice. Additionally, TPS3A notably suppressed lipogenesis and enhanced lipolysis, as shown by the downregulation of lipogenesis markers (SREBP-1 and FAS) and the upregulation of lipolysis markers (HSL and ATGL), thereby reducing renal tubular ELD in HFD-fed ApoE-/- mice and palmitic-acid-stimulated HK-2 cells. The AMPK-SIRT1-FoxO1 axis is a core signal pathway in regulating lipid deposition. Consistently, TPS3A significantly increased the levels of phosphorylated-AMPK, SIRT1, and deacetylation of Ac-FoxO1. However, these effects of TPS3A on lipogenesis and lipolysis were abolished by AMPK siRNA, SIRT1 siRNA, and FoxO1 inhibitor, resulting in exacerbated lipid deposition. Taken together, TPS3A shows promise in ameliorating renal tubular ELD by inhibiting lipogenesis and promoting lipolysis through the AMPK-SIRT1-FoxO1 signaling pathway.

Comparisons in phytochemical components and in vitro digestion properties of corresponding peels, flesh and seeds separated from two blueberry cultivars.

Highbush blueberries (HB) and rabbiteye blueberries (RB) were separated into peels, flesh, and seeds to assess the compositions of nutriment, anthocyanins, soluble sugars and fatty acids, and the in vitro digesting abilities. Total phenolics contents (TPC) of 51-56 mg GAE/g DW were found in blueberry peels. Compared with HB peels, RB peels showed much higher TPC, but only contained 35 phenolics and lacked peonidin-3-O-rutinoside. Glucose, fructose, and sucrose were all present in HB and RB, but RB flesh had a higher acid-sugar ratio. Unsaturated fatty acid concentrations in HB and RB seeds were comparable (26.65 and 26.43 mg/g, respectively). However, HB seeds have 35 fatty acids, but RB seeds lacked cis-4,7,10,13,16,19-docosahexaenoic acid and cis-10-pentadecenoic acid. The in vitro digestion test showed that the whole fruit/peels/flesh of RB had a higher recovery and bioavailability index of phenolics and anthocyanins. Therefore, the reuse of blueberry pomace needs to be emphasized. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01326-w.

Purification, structural characteristics and anti-atherosclerosis activity of a novel green tea polysaccharide.

A new homogeneous polysaccharide (TPS3A) was isolated and purified from Tianzhu Xianyue fried green tea by DEAE-52 cellulose and Sephacryl S-500 column chromatography. Structural characterization indicated that TPS3A mainly consisted of arabinose, galactose, galacturonic acid and rhamnose in a molar ratio of 5.84: 4.15: 2.06: 1, with an average molecular weight of 1.596 × 104 kDa. The structure of TPS3A was characterized as a repeating unit consisting of 1,3-Galp, 1,4-Galp, 1,3,6-Galp, 1,3-Araf, 1,5-Araf, 1,2,4-Rhap and 1-GalpA, with two branches on the C6 of 1,3,6-Galp and C2 of 1,2,4-Rhap, respectively. To investigate the preventive effects of TPS3A on atherosclerosis, TPS3A was administered orally to ApoE-deficient (ApoE-/-) mice. Results revealed that TPS3A intervention could effectively delay the atherosclerotic plaque progression, modulate dyslipidemia, and reduce the transformation of vascular smooth muscle cells (VSMCs) from contractile phenotype to synthetic phenotype by activating the expression of contractile marker alpha-smooth muscle actin (α-SMA) and inhibiting the expression of synthetic marker osteopontin (OPN) in high-fat diet-induced ApoE-/- mice. Our findings suggested that TPS3A markedly alleviated atherosclerosis by regulating dyslipidemia and phenotypic transition of VSMCs, and might be used as a novel functional ingredient to promote cardiovascular health.

Inhibition of Ca2+-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis.

The Ca2+-calpain signaling plays a pivotal role in regulating the upstream signaling pathway of cellular autophagy. The aim of the current work was to investigate the role of Ca2+-calpain signaling in the regulation of macrophage autophagy by a Laminaria japonica polysaccharide (LJP61A) in Ox-LDL induced macrophages and high fat diet fed atherosclerotic mice. Results revealed that the LJP61A markedly decreased the levels of intracellular Ca2+, calpain1, calpain2 and their downstream effectors (Gsα, cAMP and IP3), and simultaneously enhanced autophagy activity and lipid metabolism, thereby reducing lipid accumulation in the Ox-LDL stimulated macrophages and lipid-laden plaques in atherosclerotic mice. Moreover, BAPTA-AM (a Ca2+ chelator) and calpeptin (a calpain inhibitor) synergistically strengthened the beneficial effects of LJP61A on autophagy and lipid metabolism by decreasing the levels of intracellular Ca2+, calpain1, calpain2, and their downstream effectors (Gsα, cAMP and IP3) induced by Ox-LDL. These findings suggested that the LJP61A suppressed macrophage derived foam cell formation and atherosclerosis by modulating the Ca2+-calpain-mediated autophagy.

Recombinant Rice Quiescin Sulfhydryl Oxidase Strengthens the Gluten Structure through Thiol/Disulfide Exchange and Hydrogen Peroxide Oxidation.

Recombinant rice quiescin sulfhydryl oxidase (rQSOX) has the potential to improve the flour processing quality, but the mechanisms remain unclear. The effects of rQSOX on bread quality, dough rheology, and gluten structure and composition, with glucose oxidase as a positive control, were investigated. rQSOX addition could improve the dough processing quality, as proved by enhanced viscoelastic properties of dough as well as a softer crumb, higher specific volume, and lower moisture loss of bread. These beneficial effects were attributed to gluten protein polymerization and gluten network strengthening, evidenced by the improved concentration of SDS-insoluble gluten and formation of large gluten aggregates and the increased α-helix and ß-turn conformation. Furthermore, decreased free sulfhydryl and increased dityrosine in gluten as well as improved H2O2 content in dough suggested that the rQSOX dough strengthening mechanism was mainly based on the formation of disulfide bonds and dityrosine cross-links in gluten by both thiol/disulfide direct exchange and hydrogen peroxide indirect oxidation pathways.

LncRNA MALAT1 Promotes PPARα/CD36-Mediated Hepatic Lipogenesis in Nonalcoholic Fatty Liver Disease by Modulating miR-206/ARNT Axis.

Long non-coding RNAs (lncRNAs) are known to play crucial roles in nonalcoholic fatty liver disease (NAFLD). This research sought to explore mechanisms by which lncRNA MALAT1 regulates the progression of NAFLD. Thus, in order to detect the function of MALAT1 in NAFLD, in vitro and in vivo model of NAFLD were established. Then, fatty acid uptake and triglyceride level were investigated by BODIPY labeled-fatty acid uptake assay and Oil red O staining, respectively. The expressions of MALAT1, miR-206, ARNT, PPARα and CD36 were detected by western blotting and qPCR. Dual luciferase, RIP and ChIP assay were used to validate the relation among MALAT1, miR-206, ARNT and PPARα. The data revealed expression of MALAT1 was up-regulated in vitro and in vivo in NAFLD, and knockdown of MALAT1 suppressed FFA-induced lipid accumulation in hepatocytes. Meanwhile, MALAT1 upregulated the expression of ARNT through binding with miR-206. Moreover, miR-206 inhibitor reversed MALAT1 knockdown effects in decreased lipid accumulation in FFA-treated hepatocytes. Furthermore, ARNT could inhibit the expression of PPARα via binding with PPARα promoter. Knockdown of MALAT1 significantly upregulated the level of PPARα and downregulated the expression of CD36, while PPARα knockdown reversed these phenomena. MALAT1 regulated PPARα/CD36 -mediated hepatic lipid accumulation in NAFLD through regulation of miR-206/ARNT axis. Thus, MALAT1/miR-206/ARNT might serve as a therapeutic target against NAFLD.

Identification of key genes in cutaneous squamous cell carcinoma: a transcriptome sequencing and bioinformatics profiling study.

BACKGROUND: Long-term exposure to ultraviolet (UV) radiation can cause cutaneous squamous cell carcinoma (cSCC), which is one of the most common malignant cancers worldwide. Actinic keratosis (AK) is generally considered a precancerous lesion of cSCC. However, the pathogenesis and oncogenic processes of AK and cSCC remain elusive, especially in the context of photodamage. METHODS: In this study, transcriptome sequencing was performed on AK, cSCC, normal sun-exposed skin (NES) tissues, and normal non-sun-exposed skin (NNS) from 24 individuals. Bioinformatics analysis to identify the differentially expressed genes (DEGs) of 4 groups, and potential key genes of cSCC were validated by real-time quantitative reverse transcription PCR (qRT-PCR). RESULTS: A total of 46,930 genes were differentially expressed in the 4 groups, including 127 genes that were differentially expressed between NES and NNS, 420 DEGs in AK compared to NES, 1,658 DEGs in cSCC compared to NES, and 1,389 DEGs in cSCC compared to AK. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis suggested that the DEGs are involved in multiple pathways, including extracellular matrix (ECM)-receptor interaction, immune, inflammatory, microbial infection, and other related pathways. Finally, 5 new genes (HEPHL1, FBN2, SULF1, SULF2, and TCN1) were confirmed significantly upregulated in cSCC. CONCLUSIONS: Using transcriptome sequencing and integrated bioinformatical analysis, we have identified key DEGs and pathways in cSCC, which could improve our understanding of the cause and underlying molecular events of AK and cSCC. HEPHL1, FBN2, SULF1, SULF2, and TCN1 may be novel potential biomarkers and therapeutic targets of cSCC.

Polygonatum cyrtonema Hua polysaccharide exhibits anti-fatigue activity via regulating osteocalcin signaling.

In the present study, we explored the anti-fatigue activity and its potential mechanism of a purified Polygonatum cyrtonema polysaccharide (PCP) on mice using weight-loaded swimming test. Results showed that PCP remarkably prolonged the exhaustive swimming time of mice when compared with normal control group. Meanwhile, PCP decreased serum levels of lactic acid (LA), blood uric nitrogen (BUN), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA), and increased the contents of liver glycogen, muscle glycogen and muscle ATP. These results revealed that PCP had good anti-fatigue ability. The histomorphologic analysis showed that PCP increased the cross-section area of the muscle fibers. Furthermore, PCP significantly enhanced the protein levels of bone morphogenetic protein-2 (BMP-2), phosphor-Smad1, Runt-related transcription factor 2 (Runx2) and osteocalcin (OC) in skeleton. Similar variation was also observed in the expression of osteocalcin signaling mediators of phosphorylated cAMP-response element binding protein (p-CREB) and phosphorylated hormone-sensitive lipase (p-HSL) in skeletal muscle. These results suggested that PCP resisted fatigue possibly via regulating osteocalcin signaling.

Characterization of recombinant rice quiescin sulfhydryl oxidase and its improvement effect on wheat flour-processing quality.

In this study, recombinant rice quiescin sulfhydryl oxidase (rQSOX) was expressed and characterized, and its performance in flour-processing quality was further evaluated. The purified rQSOX exhibited the highest sulfhydryl oxidation activity (1.96 IU/mg) using dithiothreitol as a substrate, accompanying the production of H2O2. The optimal temperature and pH were 60 °C and pH 8.0 for rQSOX catalyzing oxidation of dithiothreitol. And rQSOX retained 50% of its maximum activity after incubation at 80 °C for 1 h. Moreover, rQSOX supplementation improved the farinograph properties of dough, indicated by the increased dough stability time and decreased degree of softening, and enhanced viscoelastic properties of the dough. Addition of rQSOX (10 IU/g flour) provided remarkable improvement in specific volume (37%) and springiness (17%) of the steamed bread, and significantly reduced the hardness by half, which was attributed to the strengthened gluten network. The results provide an understanding for rQSOX using in flour-processing industry.

Comparison of the Effects of Different Food-Grade Emulsifiers on the Properties and Stability of a Casein-Maltodextrin-Soybean Oil Compound Emulsion.

The improvement of food-grade emulsifiers in the properties and stability of complex emulsion has attracted much interest. In this study, the effects of six food-grade emulsifiers with a hydrophilic-lipophilic balance (HLB) range of 3.4-8.0 on a casein-maltodextrin-soybean oil compound emulsion were investigated by centrifugal precipitation rate (CPR), emulsifying activity index (EAI), microrheological properties, zeta potential, average particle size, and Turbiscan stability index (TSI). The optimal amounts of added succinylated monoglyceride (SMG) and polyglycerol fatty acid ester were 0.0025% and 0.1% (w/w), respectively, while that of the other four emulsifiers was 0.2% (w/w), according to the CPR. Thereinto, the SMG-stabilized emulsion exhibited the highest emulsifying activity and the lowest viscosity value and possessed the highest stability over 14 days of storage, which was indicated by the lowest TSI value and the smallest change in delta backscattering signal, relative to those of the other groups. Moreover, the emulsion stabilized by SMG displayed better emulsion stability than the control under a range of pH (6.0-8.0) and calcium ion concentrations (0-10 mM), which was attributed to the increased zeta potential value and the decreased average particle size of droplets with the addition of SMG. The present study provides a basic understanding for SMG improving the properties and stability of the complex emulsion.

Ruthenium(II) salicylate complexes inducing ROS-mediated apoptosis by targeting thioredoxin reductase.

Thioredoxin reductase (TrxR), a major component of the thioredoxin system, makes a critical role in regulating cellular redox signaling and is found to be overexpressed in many human cancer cells. TrxR has become an attractive target for anticancer agents. In this work, three Ru(II) complexes with salicylate as ligand, [Ru(phen)2(SA)] (phen = 1,10-phenanthroline, SA = salicylate, 1), [Ru(dmb)2(SA)] (dmb = 4,4'-dimethyl-2,2'-bipyridine, 2) and [Ru(bpy)2(SA)] (bpy = 2,2'-bipyridine, 3), were synthesized and characterized. The anticancer effect exerted by them was evaluated. Complex 1 was found to exhibit obvious anticancer activity, in comparison with cisplatin, against cancer cell lines, while displaying low toxicity to the normal cell line BEAS-2B. The mechanism of complex 1 cancer cell growth suppress was investigated in A549 cells. Complex 1 exerted its anticancer through inducing apoptosis and triggering cell cycle arrest at the G0/G1 phase. Complex 1 can selectively inhibit TrxR activity and thus promote the generation and accumulation of reactive oxygen species (ROS), which subsequently trigger mitochondrial dysfunction and DNA damage, activate oxidative stress-sensitive mitogen activated protein kinase (MAPK), and suppress the protein kinase B (PKB or AKT) signal pathway, resulting in apoptosis in A549 cells.

Lactose Induces Phenotypic and Functional Changes of Neutrophils and Macrophages to Alleviate Acute Pancreatitis in Mice.

Acute pancreatitis (AP) is one common clinical acute abdominal disease, for which specific pharmacological or nutritional therapies remain elusive. Lactose, a macronutrient and an inducer of host innate immune responses, possesses immune modulatory functions. The current study aimed to investigate potential modulatory effects of lactose and the interplay between the nutrient and pancreatic immunity during experimentally induced AP in mice. We found that either prophylactic or therapeutic treatment of lactose time-dependently reduced the severity of AP, as evidenced by reduced pancreatic edema, serum amylase levels, and pancreatic myeloperoxidase activities, as well as by histological examination of pancreatic damage. Overall, lactose promoted a regulatory cytokine milieu in the pancreas and reduced infiltration of inflammatory neutrophils and macrophages. On acinar cells, lactose was able to suppress caerulein-induced inflammatory signaling pathways and to suppress chemoattractant tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 production. Additionally, lactose acted on pancreas-infiltrated macrophages, increasing interleukin-10 and decreasing tumor necrosis factor alpha production. Notably, lactose treatment reversed AP-associated infiltration of activated neutrophils. Last, the effect of lactose on neutrophil infiltration was mimicked by a galectin-3 antagonist, suggesting a potential endogenous target of lactose. Together, the current study demonstrates an immune regulatory effect of lactose to alleviate AP and suggests its potential as a convenient, value-added therapeutic macronutrient to control AP, and lower the risk of its systemic complications.

[Characteristics of Ambient VOCs at the Shuangliu Site in Chengdu, China, During Summer and Autumn].

To better understand the characteristics and sources of ambient volatile organic compounds (VOCs) in a polluted area in Chengdu, which requires air pollution control, samples were collected hourly at the Shuangliu site from August 2016 to December 2016. Online gas chromatography/mass spectrometry and a flame ionization detector (GC/MS-FID) were used to analyze the mixing ratios and compositions of the VOCs. During the sampling period, the average mixing ratios of the VOCs were (45.15±43.74)×10-9. Alkanes contribute the most to the total volatile organic compounds (TVOCs), followed by aromatics (22%), halocarbon (17%), oxygenated volatile organic compounds (OVOCs; 15%), alkenes (9%), acetylene (7%), and acetonitrile (1%). Acetone, dichloromethane, acetylenes, ethylene, toluene, m/p-xylenes, propane, 1,2-dichloroethane, and methyl ethyl ketone are the dominant species. By calculating the OH loss rate, the chemical reactivity of the VOCs was estimated. Aromatics contribute the most to the total VOC reactivity, followed by alkenes. The most reactive species are styrene, m/p-xylenes, isoprene, and ethylene. Two biomass burning events were detected during the sampling period. The average mixing ratio of TVOCs is 57.65×10-9, which significantly increased during the national holiday. The mixing ratios of several C2-C5 alkenes, halocarbons, and OVOCs increased the most during the national holiday. The diurnal patterns of critical non-methane hydrocarbons (NMHCs) and OVOCs are consistent with the emission sources in this area. The VOC characteristics at the sampling site are mainly influenced by local industrial sources.

The core structure of a Dendrobium huoshanense polysaccharide required for the inhibition of human lens epithelial cell apoptosis.

The aim of this work was to investigate the core structure of a Dendrobium huoshanense polysaccharide DHPD1 required for the inhibition of lens epithelial cell apoptosis. In order to obtain the fragments containing the core domain, pectinase was employed to hydrolyze DHPD1. After 24h reaction, it is interesting that the hydrolyzation seemed to be stopped, leading to a final enzymatic fragment DHPD1-24 with molecular weight about 1552Da. Compared to DHPD1, although the bioactivity is decreased, DHPD1-24 remained the ability to inhibit the H2O2-induced apoptosis of human lens epithelial (HLE) cells via suppressing the MAPK signaling pathways. These results suggested that DHPD1-24 might be the core domain required for DHPD1 to inhibit HLE cell apoptosis. Methylation analysis showed DHPD1-24 was composed of (1→5)-linked-Araf, (1→3,6)-linked-Manp, 1-linked-Glcp, (1→4)-linked-Glcp, (1→6)-linked-Glcp, (1→4,6)-linked-Glcp, (1→6)-linked-Galp and 1-linked-Xylp in a molar ratio of 1.06:1.53:2.11:2.04:0.93:0.91:0.36:1.01. Moreover, the primary structural features of DHPD1-24 were characterized by NMR spectrum.

Neuroprotective effects of sodium hydrosulfide against ß-amyloid-induced neurotoxicity.

Alzheimer's disease (AD) is known to be caused by the accumulation of amyloid-ß peptide (Aß). The accumulation of Aß has been shown to cause learning and memory impairment in rats, and it has been shown that hydrogen sulfide donors, such as sodium hydrosulfide (NaHS) can attenuate these effects. However, the underlying mechanisms have not yet been fully eludicated. This study was designed to investigate whether NaHS attenuates the inflammation and apoptosis induced by Aß. We demonstrated that NaHS attenuated Aß25­35-induced neuronal reduction and apoptosis, and inhibited the activation of pro-caspase-3. It also decreased the protein expresion of phosphodiesterase 5 (PDE5) in the hippocampus of the rats. In addition, NaHS upregulated the expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ, but it did not affect the expression of PPAR-ß. Moreover, the Aß25­35­exposed rats exhibited a decrease in IκB-α degradation and an increase in nuclear factor-κB (NF-κB) p65 phosphorylation levels, whereas these effects were attenuated by NaHS. Our data suggest that NaHS prevents Aß-induced neurotoxicity via the upregulation of PPAR-α and PPAR-γ and the inhibition of PDE5. Hence NaHS may prove to be beneficial in the treatment of AD.

Meroterpenoids with New Skeletons from Myrtus communis and Structure Revision of Myrtucommulone K.

Five sesquiterpene-based meroterpenoids with three kinds of new skeletons [1, 2, 3, (+)-4, and (-)-4] were isolated from the leaves of Myrtus communis. Compound 1 featured a new carbon skeleton with an unprecedented octahydrospiro[bicyclo[7.2.0]undecane-2,2'-chromene] tetracyclic ring system, which possessed two preferred conformations detected by variable-temperature NMR spectroscopy experiments. In addition, the structure of reported myrtucommulone K was revised to be compound 3. The plausible biosynthetic pathways of these meroterpenoids and their cytotoxicities are discussed.

Cathelicidin-related antimicrobial peptide modulates the severity of acute pancreatitis in mice.

The present study aimed to investigate the immunomodulatory effects of mouse cathelicidin-related antimicrobial peptide (CRAMP) on experimental acute pancreatitis (AP). AP is a common clinical condition characterized by acute abdominal inflammation. Innate immune cells and mediators are intrinsically linked to the pathogenesis of AP. Cathelicidins are innate immunity-derived antimicrobial peptides that exert immunomodulatory effects on various host cells. However, how cathelicidins are involved and modulate the severity and inflammatory responses of AP remains unclear. In the present study, the mouse CRAMP gene­deficient cnlp­/­ mice and their wild­type C57BL/6J littermates were induced with AP by multiple hourly injections of supramaximal doses of caerulein. Serum amylase levels, pancreatic myeloperoxidase activity and histological examination were performed in order to determine the disease severity and the levels of inflammatory cytokines. Disease severity and inflammatory markers were subsequently evaluated in the control mice, cnlp­/­ C57BL/6J mice with AP, and wild­type C57BL/6J mice with AP. The results demonstrated that cnlp­/­ mice exhibited a more severe phenotype and inflammatory response following AP induction compared with the wild­type mice, as evidenced by increased serum amylase levels, pancreatic myeloperoxidase release, and early inflammatory mediator tumor necrosis factor­α production. Histological examination confirmed that CRAMP deficiency worsened the pancreatic inflammatory condition. These results indicate that CRAMP may be considered a novel modulatory mediator in mouse experimental AP.

Icariin, a major constituent of flavonoids from Epimedium brevicornum, protects against cognitive deficits induced by chronic brain hypoperfusion via its anti-amyloidogenic effect in rats.

Chronic cerebral hypoperfusion is considered to be a pivotal contributing factor of cognitive impairments that occur in vascular dementia and Alzheimer's disease, and ideal drug treatment for these diseases is unavailable. Hence, this study was designed to investigate the protective effects of icariin, a major constituent of flavonoids from the Chinese medicinal herb Epimedium brevicornum, on cognitive impairments and neuronal morphological damage induced by permanent occlusion of bilateral common carotid arteries (BCCAO) in rats, and further explore the potential mechanisms. This study found that BCCAO could induce cognitive deficits and neuronal morphological damage, along with deposition of beta-amyloid (Aß) in rat hippocampus. However, oral administration of icariin twice per day for 23days might attenuate cognitive deficits and neuronal morphological damage induced by BCCAO. Subsequently, icariin decreased the level of Aß in rat hippocampus subjected to BCCAO. Administration of icariin reduced the expressions of amyloid precursor protein (APP), beta-secretase 1 (BACE1), and increased the expressions of insulin-degrading enzyme (IDE) and a disintegrin and metalloproteinase domain 10 (ADAM10) in rat hippocampus. Furthermore, icariin afforded beneficial actions in suppressing transforming growth factor-ß1 (TGF-ß1) signaling via inhibition of Smad2/3 phosphorylation. In summary, icariin is effective in improving cognitive deficits and hippocampus morphological alterations subjected to BCCAO. This protection appears to be due to the decreased expressions of both APP and BACE1, and the increased expressions of both IDE and ADAM10, resulting in a decrease in the level of insoluble Aß fragments in rat hippocampus. Inhibitions of TGF-ß1 signaling and Smad2/3 phosphorylation are involved in the course.

Immunomodulatory activity and partial characterisation of polysaccharides from Momordica charantia.

Momordica charantia Linn. is used as an edible and medicinal vegetable in sub-tropical areas. Until now, studies on its composition and related activities have been confined to compounds of low molecular mass, and no data have been reported concerning the plant's polysaccharides. In this work, a crude polysaccharide of M. charantia (MCP) fruit was isolated by hot water extraction and then purified using DEAE-52 cellulose anion-exchange chromatography to produce two main fractions MCP1 and MCP2. The immunomodulatory effects and physicochemical characteristics of these fractions were investigated in vitro and in vivo. The results showed that intragastric administration of 150 or 300 mg·kg-·d⁻¹ of MCP significantly increased the carbolic particle clearance index, serum haemolysin production, spleen index, thymus index and NK cell cytotoxicity to normal control levels in cyclophosphamide (Cy)-induced immunosuppressed mice. Both MCP1 and MCP2 effectively stimulated normal and concanavalin A-induced splenic lymphocyte proliferation in vitro at various doses. The average molecular weights of MCP1 and MCP2, which were measured using high-performance gel permeation chromatography, were 8.55×104 Da and 4.41×105 Da, respectively. Both fractions exhibited characteristic polysaccharide bands in their Fourier transform infrared spectrum. MCP1 is mainly composed of glucose and galactose, and MCP2 is mainly composed of glucose, mannose and galactose. The results indicate that MCP and its fractions have good potential as immunotherapeutic adjuvants.