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GutCited

N-Acetyl Cysteine (NAC) 図

13 査読済み研究からの図表

すべて Saccharomyces boulardii Lactobacillus acidophilus Bifidobacterium lactis Lactobacillus plantarum Bifidobacterium longum Bifidobacterium bifidum Lactobacillus gasseri Bacillus coagulans Inulin Fructooligosaccharides (FOS) Galactooligosaccharides (GOS) Psyllium Husk Lactase Pancreatic Enzymes (Pancrelipase) Alpha-Galactosidase L-Glutamine N-Acetyl Cysteine (NAC) Peppermint Oil Ginger Berberine Curcumin Zinc Vitamin D Vitamin A Butyrate (Sodium/Calcium Butyrate) Omega-3 Fatty Acids (EPA/DHA) Medium-Chain Triglycerides (MCT Oil) Bovine Colostrum Aloe Vera (Inner Leaf Gel)
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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 …

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. 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 7
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Quantification of DNA double-strand break repair efficiency in H. pylori-infected gastric cells, indicating that alpha-lipoic acid supports the Ku-dependent non-homologous end joining pathway.

α-Lipoic Acid Inhibits Apoptosis by Suppressing the Loss of Ku Proteins in …

Figure 8
Figure 8 Chart

Cell viability analysis across different alpha-lipoic acid concentrations in H. pylori-infected gastric epithelial cells, establishing the effective dose range for cytoprotection.

α-Lipoic Acid Inhibits Apoptosis by Suppressing the Loss of Ku Proteins in …

Figure 4
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Oxidative stress biomarkers measured in colon, liver, and kidney tissues, comparing malondialdehyde (MDA) and glutathione (GSH) levels across treatment groups.

Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N-Acetylcysteine on Colon, Liver, …

Figure 5
Figure 5 Chart

Inflammatory cytokine levels (such as TNF-alpha, IL-6, or IL-1beta) in colonic and extraintestinal tissues, assessing whether NAC modulates systemic inflammation originating from the gut.

Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N-Acetylcysteine on Colon, Liver, …

Figure 6
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Colon length measurements and macroscopic damage scoring in the colitis model, providing gross anatomical evidence of disease severity and NAC treatment response.

Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N-Acetylcysteine on Colon, Liver, …

Figure 7
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Summary of controversial findings regarding NAC's differential effects across organs, with protective trends observed in some tissues but potential adverse signals in others.

Extraintestinal Manifestations in Induced Colitis: Controversial Effects of N-Acetylcysteine on Colon, Liver, …