Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Galectin-3 Inhibition With Modified Citrus Pectin in Hypertension.

ABSTRACT: We investigated the effect of galectin-3 (Gal-3) inhibition with modified citrus pectin on markers of collagen metabolism in a proof-of-concept randomized placebo-controlled trial of participants with elevated Gal-3 levels and hypertension. Although higher Gal-3 levels were associated with female sex, diabetes, and reduced glomerular filtration rate in cross-sectional analyses, treatment with modified citrus pectin did not change collagen markers. The effect of Gal-3 inhibition among individuals with heart failure warrants further investigation.

SUBMITTER: Lau ES

PROVIDER: S-EPMC7838053 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Galectin-3 Inhibition With Modified Citrus Pectin in Hypertension.

Lau Emily S ES Liu Elizabeth E Paniagua Samantha M SM Sarma Amy A AA Zampierollo Giovanna G López Begoña B Díez Javier J Wang Thomas J TJ Ho Jennifer E JE

JACC. Basic to translational science 20210106 1

We investigated the effect of galectin-3 (Gal-3) inhibition with modified citrus pectin on markers of collagen metabolism in a proof-of-concept randomized placebo-controlled trial of participants with elevated Gal-3 levels and hypertension. Although higher Gal-3 levels were associated with female sex, diabetes, and reduced glomerular filtration rate in cross-sectional analyses, treatment with modified citrus pectin did not change collagen markers. The effect of Gal-3 inhibition among individuals ...[more]

PMID: 33532663

Similar Datasets

Purification, chemical analysis and inhibitory effects on galectin-3 of enzymatic pH-modified citrus pectin.

Project description:Modified citrus pectin (MCP), a commercially available dietary supplement prepared from citrus pectin, contains several different polysaccharide domains, but its primary chemical structure and the binding epitopes that antagonize galectin-3 function remain unclear. In this study, five fractions were isolated from MCP after endo-polygalacturonase degradation (EMCP) and a combination of DEAE-cellulose and Sepharose CL-6B or Sephadex G-75 chromatography. Their primary structures, abilities to inhibit galectin-3-mediated hemagglutination, and antiproliferation activities on MCF-7 and A549 cell lines were studied. Results showed that EMCP-3p, one of the five fractions, was composed of Glc (89.8%), Gal (3.8%), Ara (3.1%), GalA (1.1%), Man (0.9%), and Rha (1.3%) with an average molecular weight of 88.4 KDa, which had the most substantial degree of galectin-3 inhibition with an MIC of 31.25 μg/mL, and it exhibited remarkable cytotoxicity against MCF-7 (36.7%) and A549 (57.4%) cell lines. These results provide new insight into the structure-function relationships of EMCP-derived polysaccharides.

| S-EPMC8628203 | biostudies-literature

Pectasol-C Modified Citrus Pectin targets Galectin-3-induced STAT3 activation and synergize paclitaxel cytotoxic effect on ovarian cancer spheroids.

Project description:Here we sought to determine the relationship between STAT3 activity and Galectin-3 (Gal-3) and to investigate the cytotoxic effect of PectaSol-C Modified Citrus Pectin (Pect-MCP) as a specific competitive inhibitor of Galectin-3 (Gal-3) in combination with Paclitaxel (PTX) to kill the ovarian cancer cell SKOV-3 multicellular tumor spheroid (MCTS). To this order, SKOV-3 cells in 2D and 3D cultures were treated with exogenous Gal-3 for the assessment of STAT3 activity. Two-way ANOVA main effect and IC50 of each drug Paclitaxel (PTX) and Pect-MCP or in combination were obtained from MTT assay results. The phosphorylated STAT3 levels, migration, invasion, integrin mRNA and p-AKTser473 levels were assessed in the absence or presence of each drug alone or in combination. Gal-3 expression levels were assessed in human serous ovarian cancer (SOC) specimens and its correlation with different integrin mRNA levels was further assessed. Our results showed that Gal-3 expression level was significantly increased in MCTS compared to monolayer SKOV-3 cells which triggered STAT3 phosphorylation. Moreover, Pect-MCP synergized with PTX to kill SKOV3 MCTS through abrogation of STAT3 activity and reduced expression of its downstream target HIF-1α, reduced integrin mRNA levels, and subsequently decreased AKT activity. There were higher expression levels of Gal-3 in human high-grade SOC specimens compared to the normal ovary and borderline SOC which positively and significantly correlated with α5, β2 and β6 integrin mRNA levels. Together, these results revealed for the first time that Pect-MCP could be considered as a potential drug to enhance the PTX effect on ovarian cancer cells MCTS through inhibition of STAT3 activity.

| S-EPMC6675724 | biostudies-literature

Synergistic Antioxidant and Anti-Inflammatory Effects between Modified Citrus Pectin and Honokiol.

Project description:Inflammation is a normal physiological process; however, dysregulation of this process may contribute to inflammatory-based chronic disorders and diseases in animals and humans. Therefore, the antioxidant and anti-inflammatory properties of natural products, often recognized in traditional medicine systems, represent therapeutic modalities to reduce or prevent uncontrolled inflammatory processes which in turn potentially ameliorate or prevent sequelae of inflammatory-based symptoms of chronic diseases. We have investigated the antioxidant and anti-inflammatory effects of honokiol (HNK) and modified citrus pectin (MCP) in vitro and examined whether the MCP?:?HNK combination has synergistic effects on antioxidant and anti-inflammatory properties. Although both HNK and MCP induced a dose-dependent increase in antioxidant activity, the latter has a consistently higher antioxidant effect. The MCP?:?HNK (9?:?1) combination induced a synergistic effect on antioxidant activity suggesting that the combination is significantly more efficacious than individual compounds. In mouse monocytes, the lipopolysaccharide- (LPS-) induced tumor necrosis-? (TNF-?) synthesis was significantly inhibited by HNK and the MCP?:?HNK combination in a dose-dependent manner and synergistic effects were clearly demonstrated with the combination on TNF-? inhibition. This combination effect was also evident on inhibition of nuclear factor-kappa B activity, cyclooxygenase-II activity, and lipid peroxidation in mouse monocytes. Further research into the combination is warranted.

| S-EPMC5576403 | biostudies-literature

Citrus pectin modified by microfluidization and ultrasonication: Improved emulsifying and encapsulation properties.

Project description:In this study, modified citrus pectin treated with a combination of microfluidization and ultrasonication was compared to the original and ultrasonication treated pectin on hydrodynamic diameter, molecular weight, polydispersity, zeta potential, apparent viscosity, Fourier-transform infrared spectroscopy (FTIR), 2,2-diphenyl-1-picryl hydrazyl (DPPH) radical scavenging capacity, scanning electron microscope (SEM), atomic force microscopy (AFM), their emulsifying properties and encapsulation properties. Modified pectin treated with a combination of microfluidization and moderate ultrasonication (MUB) was found to have lowest hydrodynamic diameter (418 nm), molecular weight (237.69 kDa) and polydispersity (0.12), and relatively low apparent viscosity among all pectin samples. Furthermore, it showed significantly higher DPPH radical scavenging capacity than the original pectin although only slightly higher than that of ultrasonication treated one (UB). MUB showed a thin fibrous morphology and decreased degree of branching from SEM and AFM. Emulsion stabilized by MUB had highest centrifugal and thermal stability compared to emulsions stabilized by UB and the original pectin. This could be attributed to higher interfacial loading of MUB (17.90 mg/m2) forming more compact interfacial layer observed by confocal laser scanning microscopy (CLSM). Moreover, both MUB and UB exhibited improved encapsulation functionality to protect cholecalciferol (vitamin D3) from UV degradation compared to the original pectin.

| S-EPMC7786527 | biostudies-literature

Heat-modified citrus pectin induces apoptosis-like cell death and autophagy in HepG2 and A549 cancer cells.

Project description:Cancer is still one of the leading causes of death worldwide, and finding new treatments remains a major challenge. Previous studies showed that modified forms of pectin, a complex polysaccharide present in the primary plant cell wall, possess anticancer properties. Nevertheless, the mechanism of action of modified pectin and the pathways involved are unclear. Here, we show that citrus pectin modified by heat treatment induced cell death in HepG2 and A549 cells. The induced cell death differs from classical apoptosis because no DNA cleavage was observed. In addition, Z-VAD-fmk, a pan-caspase inhibitor, did not influence the observed cell death in HepG2 cells but appeared to be partly protective in A549 cells, indicating that heat-modified citrus pectin might induce caspase-independent cell death. An increase in the abundance of the phosphatidylethanolamine-conjugated Light Chain 3 (LC3) protein and a decrease in p62 protein abundance were observed in both cell types when incubated in the presence of heat-modified citrus pectin. These results indicate the activation of autophagy. To our knowledge, this is the first time that autophagy has been revealed in cells incubated in the presence of a modified form of pectin. This autophagy activation appears to be protective, at least for A549 cells, because its inhibition with 3-methyladenine increased the observed modified pectin-induced cytotoxicity. This study confirms the potential of modified pectin to improve chemotherapeutic cancer treatments.

| S-EPMC4368604 | biostudies-literature

Migration and proliferation of cancer cells in culture are differentially affected by molecular size of modified citrus pectin.

Project description:While chemically and thermally modified citrus pectin (MCP) has already been studied for health benefits, it is unknown how size-fractionated oligo- and polysaccharides differentially affect cancer cell behavior. We produced thermally MCP and fractionated it by molecular size to evaluate the effect these polymers have on cancer cells. MCP30/10 (between 30 and 10?kDa) had more esterified homogalacturonans (HG) and fewer rhamnogalacturonans (RG-I) than MCP and MCP30 (higher than 30?kDa), while MCP10/3 (between 10 and 3?kDa) showed higher amounts of type I arabinogalactans (AGI) and lower amounts of RG-I. MCP3 (smaller than 3?kDa) presented less esterified HG and the lowest amount of AGI and RG-I. Our data indicate that the enrichment of de-esterified HG oligomers and the AGI and RG-I depletions in MCP3, or the increase of AGI and loss of RGI in MCP30/10, enhance the anticancer behaviors by inhibiting migration, aggregation, and proliferation of cancer cells.

| S-EPMC6886127 | biostudies-literature

Modified Citrus Pectin Treatment in Non-Metastatic Biochemically Relapsed Prostate Cancer: Results of a Prospective Phase II Study.

Project description:Optimal therapy of biochemically relapsed prostate cancer (BRPC) after local treatment is elusive. An established modified citrus pectin (PectaSol®, P-MCP), a dietary polysaccharide, is an established antagonist of galectin-3, a carbohydrate-binding protein involved in cancer pathogenesis. Based on PSA dynamics, we report on the safety and the primary outcome analysis of a prospective phase II study of P-MCP in non-metastatic BRPC based. Sixty patients were enrolled, and one patient withdrew after a month. Patients (n = 59) were given P-MCP, 4.8 grams X 3/day, for six months. The primary endpoint was the rate without PSA progression and improved PSA doubling time (PSADT). Secondary endpoints were the rate without radiologic progression and toxicity. Patients that did not progress by PSA and radiologically at six months continued for an additional twelve months. After six months, 78% (n = 46) responded to therapy, with a decreased/stable PSA in 58% (n = 34), or improvement of PSADT in 75% (n = 44), and with negative scans, and entered the second twelve months treatment phase. Median PSADT improved significantly (p = 0.003). Disease progression during the first 6 months was noted in only 22% (n = 13), with PSA progression in 17% (n = 10), and PSA and radiologic progression in 5% (n = 3). No patients developed grade 3 or 4 toxicity.

| S-EPMC8706421 | biostudies-literature

Marine Microalgae, Spirulina maxima-Derived Modified Pectin and Modified Pectin Nanoparticles Modulate the Gut Microbiota and Trigger Immune Responses in Mice.

Project description:This study evaluated the modulation of gut microbiota, immune responses, and gut morphometry in C57BL/6 mice, upon oral administration of S. maxima-derived modified pectin (SmP, 7.5 mg/mL) and pectin nanoparticles (SmPNPs; 7.5 mg/mL). Metagenomics analysis was conducted using fecal samples, and mice duodenum and jejunum were used for analyzing the immune response and gut morphometry, respectively. The results of metagenomics analysis revealed that the abundance of Bacteroidetes in the gut increased in response to both modified SmP and SmPNPs (75%) as compared with that in the control group (66%), while that of Firmicutes decreased in (20%) as compared with that in the control group (30%). The mRNA levels of mucin, antimicrobial peptide, and antiviral and gut permeability-related genes in the duodenum were significantly (p < 0.05) upregulated (> 2-fold) upon modified SmP and SmPNPs feeding. Protein level of intestinal alkaline phosphatase was increased (1.9-fold) in the duodenum of modified SmPNPs feeding, evidenced by significantly increased goblet cell density (0.5 ± 0.03 cells/1000 µm2) and villi height (352 ± 10 µm). Our results suggest that both modified SmP and SmPNPs have the potential to modulate gut microbial community, enhance the expression of immune related genes, and improve gut morphology.

| S-EPMC7143556 | biostudies-literature

Citrus Pectin-Derived Carbon Microspheres with Superior Adsorption Ability for Methylene Blue.

Project description:In this study, citrus pectin-derived, green, and tunable carbon microspheres with superior adsorption capacity and high adsorption rate, as well as good reusability toward methylene blue adsorption, were prepared by a facile hydrothermal method without any hazardous chemicals. The materials hold great potential for the treatment of methylene blue wastewater.

| S-EPMC5535227 | biostudies-literature

Eudragit S100 Coated Citrus Pectin Nanoparticles for Colon Targeting of 5-Fluorouracil.

Project description:In the present study, Eudragit S100 coated Citrus Pectin Nanoparticles (E-CPNs) were prepared for the colon targeting of 5-Fluorouracil (5-FU). Citrus pectin also acts as a ligand for galectin-3 receptors that are over expressed on colorectal cancer cells. Nanoparticles (CPNs and E-CPNs) were characterized for various physical parameters such as particle size, size distribution, and shape etc. In vitro drug release studies revealed selective drug release in the colonic region in the case of E-CPNs of more than 70% after 24 h. In vitro cytoxicity assay (Sulphorhodamine B assay) was performed against HT-29 cancer cells and exhibited 1.5 fold greater cytotoxicity potential of nanoparticles compared to 5-FU solution. In vivo data clearly depicted that Eudragit S100 successfully guarded nanoparticles to reach the colonic region wherein nanoparticles were taken up and showed drug release for an extended period of time. Therefore, a multifaceted strategy is introduced here in terms of receptor mediated uptake and pH-dependent release using E-CPNs for effective chemotherapy of colorectal cancer with uncompromised safety and efficacy.

| S-EPMC5455456 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data