| In Vitro |
Alginate oligosaccharides (1 mg/mL) attenuate MSU-induced ROS overproduction in primary mouse bone marrow-derived macrophages[1].
Alginate oligosaccharides (0.5-2%; 6-52 h) improve colistin diffusion through artificial sputum medium in a concentration-dependent manner[2].
Alginate oligosaccharides (0.5-2%; 28 h) enhance colistin-mediated reduction in ATP production of Pseudomonas aeruginosa NH57388A planktonic cells[2].
Alginate oligosaccharides (1%; 24 h) enhance colistin-mediated disruption and cell death of Pseudomonas aeruginosa NH57388A biofilms[2].
Alginate oligosaccharides (1% surface treatment; 24 h incubation with colistin) enhance colistin-mediated reduction in cell density of Pseudomonas aeruginosa NH57388A planktonic and attached biofilm cells at a colistin concentration of 60 µg/mL[2].
Alginate oligosaccharides (0.5-6%; 48 h) synergistically enhances the antifungal activity of nystatin against planktonic Candida spp., including a 32-fold reduction in Nystatin (HY-17409) MIC for C. dubliniensis 40/01a when treated with 6% OligoG, an effect that persists in the presence of exogenous ergosterol[3].
Alginate oligosaccharides (2-6%; 48 h) alone significantly inhibits planktonic growth of C. parapsilosis W23 and C. auris NCPF 8971, and enhances the growth-inhibitory effect of nystatin for these two strains, but not for C. albicans ATCC 90028 or C. albicans GBJ 13/4A[3].
Alginate oligosaccharides (250-500 µg/mL; 24 h) significantly reduce nitric oxide production in LPS (HY-D1056)-stimulated murine RAW 264.7 macrophages[4].
Alginate oligosaccharides (125-500 µg/mL; 24 h) reduce proinflammatory cytokine (IL-1β, IL-6, TNF-α) levels and increase anti-inflammatory cytokine (IL-10) levels in LPS-stimulated murine RAW 264.7 macrophages and bone-marrow-derived macrophages[4].
Alginate oligosaccharides (125-500 µg/mL; 24 h) activate AMPK phosphorylation and inhibit NF-κB p65 phosphorylation in LPS-stimulated murine RAW 264.7 macrophages and bone-marrow-derived macrophages[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Alginate oligosaccharides Related Antibodies
Cell Viability Assay[2]
| Cell Line: |
Pseudomonas aeruginosa NH57388A biofilms and planktonic cells |
| Concentration: |
0.5% (pre-incubated); 1% (pre-incubated, surface treatment); 2% (pre-incubated); 60 µg/mL colistin |
| Incubation Time: |
4 h (pre-incubation); 24 h (incubation with colistin) |
| Result: |
Combined with 60 µg/mL colistin, caused a significant reduction in ATP production for total planktonic cells at 1% or 2% concentrations (either surface treatment or pre-incubation).
Combined with 60 µg/mL colistin, caused a significant reduction in ATP production for attached biofilm cells at 0.5% or 1% concentrations (either surface treatment or pre-incubation). |
Others (Confocal laser scanning microscopy LIVE/DEAD assay)[2]
| Cell Line: |
Pseudomonas aeruginosa NH57388A biofilms |
| Concentration: |
1% (surface treatment); 40 µg/mL, 60 µg/mL colistin |
| Incubation Time: |
24 h (incubation with colistin) |
| Result: |
Caused a substantial reduction in biofilm thickness and a significantly larger increase in bacterial cell death (p < 0.05 compared to untreated control).
Resulted in a higher dead/live cell ratio than colistin alone at 40 µg/mL and 60 µg/mL. |
Others (Bacterial cell density assay)[2]
| Cell Line: |
Pseudomonas aeruginosa NH57388A biofilms and planktonic cells |
| Concentration: |
1% (surface treatment); 60 µg/mL colistin |
| Incubation Time: |
24 h (incubation with colistin) |
| Result: |
Combined with 60 µg/mL colistin, caused a significant decrease in bacterial cell density for planktonic supernatant cells, washed planktonic cells, total planktonic cells, and attached biofilm cells. |
Cell Viability Assay[4]
| Cell Line: |
murine RAW 264.7 macrophages, bone-marrow-derived macrophages (BMDMs) |
| Concentration: |
125, 250, 500 µg/mL |
| Incubation Time: |
24 h (AOS preincubation); 24 h (LPS incubation after AOS preincubation) |
| Result: |
Exhibited no effect on the viability of either RAW 264.7 cells or BMDMs, regardless of LPS stimulation. |
Others (Nitric Oxide Measurement)[4]
| Cell Line: |
murine RAW 264.7 macrophages |
| Concentration: |
125, 250, 500 µg/mL AOS; 1 µg/mL LPS |
| Incubation Time: |
24 h (AOS preincubation); 24 h (LPS incubation after AOS preincubation) |
| Result: |
Significantly inhibited LPS-induced NO production relative to LPS treatment alone at 250 and 500 µg/mL. |
ELISA Assay[4]
| Cell Line: |
murine RAW 264.7 macrophages, bone-marrow-derived macrophages (BMDMs) |
| Concentration: |
125, 250, 500 µg/mL AOS; 1 µg/mL LPS |
| Incubation Time: |
24 h (AOS preincubation); 24 h (LPS incubation after AOS preincubation) |
| Result: |
Significantly inhibited LPS-induced IL-6 secretion at 250 and 500 µg/mL in RAW 264.7 cells.
Significantly decreased IL-1β and TNF-α levels at 125 and 250 µg/mL in RAW 264.7 cells.
Significantly enhanced IL-10 secretion at 250 µg/mL relative to LPS alone in RAW 264.7 cells.
Significantly reduced LPS-induced proinflammatory cytokine release (IL-1β, IL-6, TNF-α) at 125, 250, and 500 µg/mL in BMDMs.
Increased IL-10 production relative to LPS treatment alone at 125, 250, and 500 µg/mL in BMDMs. |
Western Blot Analysis[4]
| Cell Line: |
murine RAW 264.7 macrophages, bone-marrow-derived macrophages (BMDMs) |
| Concentration: |
125, 250, 500 µg/mL AOS; 1 µg/mL LPS |
| Incubation Time: |
24 h (AOS preincubation); 1 h (LPS incubation after AOS preincubation) |
| Result: |
Significantly upregulated p-AMPK levels at 125, 250, and 500 µg/mL in RAW 264.7 cells.
Significantly suppressed p-NF-κB p65 levels at 250 and 500 µg/mL relative to LPS alone in RAW 264.7 cells.
Significantly increased p-AMPK levels at 125, 250, and 500 µg/mL in BMDMs.
Inhibited NF-κB p65 phosphorylation relative to LPS treatment alone at 125, 250, and 500 µg/mL in BMDMs. |
|
| In Vivo |
Alginate oligosaccharides (100-400 mg/kg; i.p., o.g.; multiple administration regimens) ameliorates gouty arthritis in mice via Nrf2-dependent antioxidant signaling, suppressing ROS-mediated NLRP3 inflammasome activation and TRPV1 channel enhancement, with significant dose-dependent reductions in joint swelling, pain, inflammation, and oxidative stress[1].
Alginate oligosaccharides (400-800 mg/kg; p.o.; daily; 14 days) alleviate DSS (HY-116282C)-induced ulcerative colitis in male C57BL/6 mice, with the 600 mg/kg dose showing superior efficacy across multiple endpoints including DAI score reduction, histological damage improvement, cytokine modulation, AMPK activation, NF-κB inhibition, and gut microbiota restoration[4].
Alginate oligosaccharides (200 mg/kg; p.o.; daily; 28 days) alleviates Fumonisin B1 (HY-N6719)-induced intestinal damage, inflammation, oxidative stress, and gut dysbiosis in female C57BL/6J mice by promoting gut microbiota homeostasis, increasing beneficial microbial abundance and short-chain fatty acid production, enhancing intestinal barrier function, and reducing epithelial cell apoptosis[5].
Alginate oligosaccharides (200 mg/kg; p.o.; daily; 28 days) promotes intestinal development, increases beneficial gut microbial abundance and short-chain fatty acid production, enhances intestinal mucus barrier function, and improves oxidative stress markers in healthy female C57BL/6J mice[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: |
C57BL/6J (male, 6-8 weeks old); Ly6G-IRES-GFP knock-in (male); Nrf2 knockout (Nrf2-/-, male, generated via Cas9-associated gRNA technique)[1] |
| Dosage: |
AOS2: 200 mg/kg; AOS3: 100-400 mg/kg; AOS4: 200 mg/kg |
| Administration: |
i.p. (3 administrations: 1 h pre-MSU, 5 h post-MSU, 23 h post-MSU); i.p. (4 administrations: 1 h pre-MSU, 5 h post-MSU, 23 h post-MSU, 47 h post-MSU for 48 h time point); o.g. (2 administrations: 5 h post-MSU, 23 h post-MSU) |
| Result: |
Significantly reduced MSU-induced ankle swelling (AOS2, AOS3, AOS4 at 200 mg/kg, i.p.).
Produced the most effective alleviation of mechanical allodynia (AOS2 and AOS3 at 200 mg/kg, i.p.), while AOS4 showed less effect.
Dose-dependently reduced joint edema (AOS3 at 100-400 mg/kg, i.p.); significantly alleviated mechanical allodynia (AOS3 at 200 and 400 mg/kg, i.p.), while 100 mg/kg did not.
Reduced heat hyperalgesia, improved gait impairments (normalized paw area, swing, and stride length ratios at 8 h and 24 h post-MSU), and did not alter locomotor activity (AOS3 at 200 mg/kg, i.p.).
Significantly ameliorated mechanical allodynia (AOS3 at 200 mg/kg, o.g. administered post-MSU).
Reduced MSU-induced overexpression of NLRP3 inflammasome components (NLRP3, cleaved Caspase-1, ASC, cleaved IL-1β) in ankle joint tissues, and attenuated upregulation of pro-inflammatory cytokines (Il1b, Tnfa, Il6, Cxcl2) (AOS3 at 200 mg/kg, i.p.).
Restored SOD and GSH-Px activities, reduced MDA and H2O2 levels, and decreased in vivo ROS production (measured via L-012 chemiluminescence) in ankle joints of model mice (AOS3 at 200 mg/kg, i.p.).
Promoted Nrf2 nuclear translocation in ankle joint tissues; failed to alleviate mechanical allodynia, joint edema, oxidative stress, or NLRP3 inflammasome overexpression in Nrf2-/- mice (AOS3 at 200 mg/kg, i.p.).
Reduced inflammatory cell infiltration (including neutrophils) in ankle joints (AOS3 at 200 mg/kg, i.p.).
Attenuated enhanced TRPV1 channel function in DRG neurons (reduced capsaicin-induced Ca2+ transients, percentage of capsaicin-responsive neurons, action potential generation, and membrane depolarization) and reduced neuropeptide (CGRP, Substance P) levels in ankle joint tissues (AOS3 at 200 mg/kg, i.p.). |
| Animal Model: |
C57BL/6 (8-week-old male; DSS-induced colitis)[4] |
| Dosage: |
400 mg/kg; 600 mg/kg; 800 mg/kg |
| Administration: |
p.o.; daily; 14 days |
| Result: |
Reduced DSS-induced body weight loss at 400 mg/kg and 600 mg/kg.
Significantly reduced disease activity index (DAI) scores at 600 mg/kg.
Significantly improved DSS-induced colon shortening at 400 mg/kg and 600 mg/kg.
Significantly improved rectal bleeding at 600 mg/kg and 800 mg/kg.
Improved DSS-induced colonic histological damage, with significant reductions in colonic histological scores at 600 mg/kg and 800 mg/kg.
Improved DSS-induced ileal histological damage, with significant reductions in ileal histological scores at 600 mg/kg and 800 mg/kg.
Significantly reduced serum levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α at all three doses.
Significantly reduced serum IFN-γ levels and increased serum IL-10 levels at 600 mg/kg and 800 mg/kg.
Significantly increased AMPK phosphorylation in colonic tissues at 600 mg/kg.
Significantly reduced NF-κB p65 phosphorylation in colonic tissues at all three doses.
Significantly increased gut microbiota Shannon index at 600 mg/kg.
Shifted gut microbial community structure closer to the control group, reversed DSS-induced increases in Proteobacteria and Epsilonbacteraeota relative abundance and decreases in Bacteroidetes relative abundance, increased Ruminococcaceae relative abundance, and increased relative abundances of probiotic genera Ruminococcaceae_UCG-005 and Alistipes at 600 mg/kg. |
| Animal Model: |
C57BL/6J (female, 8 weeks old, fumonisin B1-induced intestinal damage model)[5] |
| Dosage: |
200 mg/kg |
| Administration: |
p.o.; daily; 28 days |
| Result: |
Increased body weight gain, small intestine weight, and colon weight compared to controls when administered alone.
Increased cecal concentrations of total SCFAs, acetate, propionate, and butyrate when administered alone.
Increased relative abundance of beneficial gut microbes including Turicibacter, Roseburia, Bifidobacterium, and Akkermansia in cecal digesta, and Bifidobacterium, Romboutsia, Muribaculum, Coriobacteriaceae_UCG_002, Negativibacillus, and Parasutterella in feces when administered alone.
Increased ileal and colonic goblet cell counts when administered alone.
Increased ileal mRNA levels of MUC1, MUC2, MUC3, and colonic mRNA levels of MUC1, MUC2, MUC3 when administered alone.
Increased plasma IL-10 and T-SOD levels, decreased plasma MDA levels when administered alone.
Restored body weight gain to match AOS-only levels when combined with FB1.
Increased colon weight compared to FB1-only mice when combined with FB1.
Reduced ileal and colonic intestinal damage scores compared to FB1-only mice when combined with FB1.
Reversed FB1-induced reductions in ileal and colonic goblet cell counts when combined with FB1.
Increased ileal MUC2 mRNA levels and colonic MUC1, MUC2, MUC3 mRNA levels compared to FB1-only mice when combined with FB1.
Reduced FB1-induced increases in colonic TUNEL-positive apoptotic cells when combined with FB1.
Decreased ileal CASP3 mRNA levels and increased colonic CASP1, BAX, BCL2, and LC3B mRNA levels compared to FB1-only mice when combined with FB1.
Reversed FB1-induced gut microbiota dysbiosis, with increased relative abundance of Turicibacter, Roseburia, and Rhodococcus in cecal digesta, and Roseburia and Parasutterella in feces compared to FB1-only mice when combined with FB1.
Increased cecal propionate and butyrate levels, and reversed FB1-induced reductions in cecal propionate levels when combined with FB1.
Increased fecal propionate and butyrate levels compared to FB1-only mice when combined with FB1.
Decreased FB1-induced increases in ileal MYD88, IL-1β, and IL-6 mRNA levels when combined with FB1.
Increased colonic IL-10 mRNA levels and decreased colonic NLRP3 mRNA levels compared to FB1-only mice when combined with FB1.
Increased ileal and colonic CLDN1, OCLN, and ZO-1 mRNA levels compared to FB1-only mice when combined with FB1.
Increased plasma IL-10 and T-SOD levels, and decreased plasma IL-1β, IL-6, TNF-α, IFN-γ, and MDA levels compared to FB1-only mice when combined with FB1. |
| Animal Model: |
C57BL/6J (female, 8 weeks old)[5] |
| Dosage: |
200 mg/kg |
| Administration: |
p.o.; daily; 28 days |
| Result: |
Increased body weight gain, small intestine weight, and colon weight compared to controls.
Increased cecal concentrations of total SCFAs, acetate, propionate, and butyrate.
Increased relative abundance of beneficial gut microbes including Turicibacter, Roseburia, Bifidobacterium, and Akkermansia in cecal digesta, and Bifidobacterium, Romboutsia, Muribaculum, Coriobacteriaceae_UCG_002, Negativibacillus, and Parasutterella in feces.
Increased ileal and colonic goblet cell counts.
Increased ileal mRNA levels of MUC1, MUC2, MUC3, and colonic mRNA levels of MUC1, MUC2, MUC3.
Increased plasma IL-10 and T-SOD levels, decreased plasma MDA levels. |
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