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N-Acetyl Cysteine (NAC) Hình ảnh

43 hình ảnh từ nghiên cứu có bình duyệt

Tất cả Psyllium Husk Bifidobacterium lactis Fructooligosaccharides (FOS) Lactobacillus plantarum Peppermint Oil Pancreatic Enzymes (Pancrelipase) Curcumin Vitamin A Medium-Chain Triglycerides (MCT Oil) Galactooligosaccharides (GOS) Lactobacillus gasseri Aloe Vera (Inner Leaf Gel) Alpha-Galactosidase Vitamin D L-Glutamine Inulin Ginger Lactase Berberine Omega-3 Fatty Acids (EPA/DHA) Bovine Colostrum Zinc Bifidobacterium bifidum Butyrate (Sodium/Calcium Butyrate) Bacillus coagulans Saccharomyces boulardii Lactobacillus acidophilus N-Acetyl Cysteine (NAC) Bifidobacterium longum
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Fig. 1 Schematic illustration of turmeric-derived nanoparticles (TDNPs 2) isolation and targeted ulcerative colitis (UC) therapy via oral administration. A TDNPs 2 were isolated and purified from edible turmeric by ultracentrifugation and sucrose gradient
Figure 1 Diagram

Turmeric-derived nanoparticles (TDNPs 2) are isolated through sucrose gradient ultracentrifugation and administered orally to target inflamed colonic tissue in a murine colitis model. The schematic outlines the isolation workflow from edible turmeric to purified nanovesicles.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 2 Characterization of TDNPs. A TDNPs were isolated and purified by sucrose gradient ultracentrifugation, band 1 from 8%/30% interface was named TDNPs 1, and band 2 from 30%/45% interface was named TDNPs 2. B Transmission Electron Microscopy (TEM) to
Figure 2 Chart

Characterization of turmeric-derived nanoparticles reveals two distinct bands (TDNPs 1 and TDNPs 2) at the 8%/30% and 30%/45% sucrose gradient interfaces, respectively. TDNPs 2 demonstrate appropriate size distribution and surface charge for oral drug delivery applications.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Figure 3
Figure 3 Chart

In vitro assessment of turmeric-derived nanovesicles demonstrates anti-inflammatory activity, including suppression of pro-inflammatory cytokine production in activated macrophages. Dose-dependent reductions in TNF-alpha and IL-6 secretion are observed.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 4 TDNPs 2 preferentially localized to the inflamed colon. A Digestive tract, mesenteric lymph nodes (MLN), and vital organs (Heart, liver, spleen, lung, kidney, and) were imaged by IVIS® Spectrum imaging system. B–D FACS was used to determine the pop
Figure 4 Photograph

Biodistribution imaging using IVIS Spectrum reveals that TDNPs 2 preferentially accumulate in inflamed colonic tissue following oral administration. Fluorescence signals are minimal in non-target organs including heart, liver, spleen, lung, and kidney.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Figure 5
Figure 5 Chart

Oral TDNPs 2 administration significantly attenuates disease activity index scores and colon shortening in DSS-induced colitis mice. Body weight recovery is also improved compared to untreated colitis controls.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Figure 6
Figure 6 Chart

Intestinal permeability assessment indicates that TDNPs 2 treatment preserves gut barrier integrity in colitis mice. Tight junction protein expression, including ZO-1 and occludin, is maintained at near-normal levels.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 7 Histological stain to evaluate the protective effect of TDNPs 2 on colitis. A Representative H&E-stained colon. Inflammatory cell infiltration was indicated by arrowheads. B Colonic goblet cells were stained by Alcian blue. As goblet cells prod
Figure 7 Micrograph

Histological examination with H&E staining reveals markedly reduced inflammatory cell infiltration and preserved goblet cell density in TDNPs 2-treated colitic mice. Colonic tissue architecture remains largely intact compared to severe disruption in untreated animals.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 8 Oral administration of TDNPs 2 accelerated inflammation resolution of colitis. A ECIS wound healing assay. B Lcn-2 quantification (n= 5).
Figure 8 Chart

Wound healing assays and fecal lipocalin-2 quantification demonstrate that TDNPs 2 accelerate resolution of intestinal inflammation. Lcn-2 levels, a sensitive marker of intestinal inflammation, decrease significantly with treatment.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 9 Biocompatibility evaluation of TDNPs 2. A Vital organs weights (n= 5). B Pro-inflammatory cytokines (n= 5). C Indicators reflected the physiological function of the liver were evaluated. D H&E staining, scale bar: 50 μm
Figure 9 Chart

Biocompatibility evaluation shows no significant changes in vital organ weights, pro-inflammatory cytokines, or liver function indicators in TDNPs 2-treated mice. H&E staining of major organs confirms absence of toxicity.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Fig. 10 TDNPs 2 exerted a protective effect by inactivating the NF-κB pathway. A NF-κB activity evaluation (n= 5). B Phospho-NF-κB p65 expression was evaluated by ELISA assay (n= 5). C The translocation of NF-kB-p65 to the nucleus was assessed by immunofl
Figure 10 Chart

TDNPs 2 exert their protective effect at least partly through inactivation of the NF-kB signaling pathway. Reduced phospho-NF-kB p65 expression and decreased nuclear translocation indicate suppression of this key inflammatory cascade.

Oral administration of turmeric-derived exosome-like nanovesicles with anti-inflammatory and pro-resolving bioactions for …

Figure 3
Figure 3 Diagram

Mechanistic diagram illustrating the role of ferroptosis — characterized by iron accumulation, lipid peroxidation, and ROS production — in the pathogenesis of inflammatory bowel disease and its potential as a therapeutic target.

Role of ferroptosis in the pathogenesis and as a therapeutic target of …

Figure 4
Figure 4 Diagram

Mechanistic diagram illustrating the role of ferroptosis — characterized by iron accumulation, lipid peroxidation, and ROS production — in the pathogenesis of inflammatory bowel disease and its potential as a therapeutic target.

Role of ferroptosis in the pathogenesis and as a therapeutic target of …

Figure 5
Figure 5 Diagram

Mechanistic diagram illustrating the role of ferroptosis — characterized by iron accumulation, lipid peroxidation, and ROS production — in the pathogenesis of inflammatory bowel disease and its potential as a therapeutic target.

Role of ferroptosis in the pathogenesis and as a therapeutic target of …

Figure 6
Figure 6 Diagram

Mechanistic diagram illustrating the role of ferroptosis — characterized by iron accumulation, lipid peroxidation, and ROS production — in the pathogenesis of inflammatory bowel disease and its potential as a therapeutic target.

Role of ferroptosis in the pathogenesis and as a therapeutic target of …

Figure 4
Figure 4

Increased susceptibility of IDH2-deficient mice to dextran sodium sulfate-induced colitis.

Figure 5
Figure 5

Increased susceptibility of IDH2-deficient mice to dextran sodium sulfate-induced colitis.

Figure 6
Figure 6

Increased susceptibility of IDH2-deficient mice to dextran sodium sulfate-induced colitis.

Figure 7
Figure 7

Increased susceptibility of IDH2-deficient mice to dextran sodium sulfate-induced colitis.

Figure 5
Figure 5

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

Figure 6
Figure 6

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

Figure 3 Histological examinations of effects of selenium-containing amino acids on DSS-induced IBD in mice. (A) Representative H&E-stained colon sections of each group (scale bar, 200 μm); (B) Histological scoring of mice treated with selenium-contai
Figure 7

Figure 3 Histological examinations of effects of selenium-containing amino acids on DSS-induced IBD in mice. (A) Representative H&E-stained colon sections of each group (scale bar, 200 μm); (B) Histological scoring …

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

Figure 8
Figure 8

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

Figure 9
Figure 9

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

Figure 6 Effects of selenium-containing amino acids on biochemical test parameters in DSS-induced IBD in mice. Serum levels of (A) ALT, (B) AST, (C) BUN, and (D) CRE in different groups. Differences were assessed via one-way analysis of variance (ANOVA) w
Figure 10

Figure 6 Effects of selenium-containing amino acids on biochemical test parameters in DSS-induced IBD in mice. Serum levels of (A) ALT, (B) AST, (C) BUN, and (D) CRE in different …

Selenium-Containing Amino Acids Protect Dextran Sulfate Sodium-Induced Colitis via Ameliorating Oxidative Stress …

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