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477 सहकर्मी-समीक्षित शोध से आंकड़े

सभी 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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Figure 5
Figure 5 Micrograph

Histological analysis of colonic tissue reveals the extent of inflammatory infiltration and mucosal damage. This figure compares histopathological scores across treatment groups in the acute experimental colitis model.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 6
Figure 6 Chart

Pro-inflammatory cytokine levels in colonic tissue were quantified to assess the anti-inflammatory effects of C. butyricum treatment. This figure presents TNF-alpha, IL-6, and IL-1beta expression data across experimental groups.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 7
Figure 7 Chart

Tight junction protein expression indicates intestinal barrier integrity. This figure shows changes in occludin, claudin, and ZO-1 levels in colonic tissue following C. butyricum or vesicle treatment.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 8
Figure 8 Chart

Gut microbiome composition was analyzed to determine how C. butyricum treatment modulates the intestinal microbial community. This figure presents 16S rRNA sequencing data showing microbial diversity and taxonomic abundance.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 9
Figure 9 Chart

Alpha and beta diversity metrics reveal shifts in gut microbial community structure following probiotic intervention. This figure compares microbiome diversity indices between C. butyricum-treated and control groups.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 10
Figure 10 Chart

Specific bacterial taxa were differentially abundant in C. butyricum-treated mice compared to controls. This figure highlights the key microbial shifts associated with amelioration of colitis symptoms.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 11
Figure 11 Chart

Short-chain fatty acid production in the gut is modulated by C. butyricum colonization. This figure presents metabolomic data on butyrate and other SCFA concentrations in the colonic lumen.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 12
Figure 12 Chart

Signaling pathway analysis reveals molecular mechanisms underlying C. butyricum's protective effects. This figure presents Western blot or gene expression data for key inflammatory and barrier-related signaling pathways.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 13
Figure 13 Chart

Extracellular vesicles from C. butyricum may directly modulate intestinal epithelial cell responses. This figure presents in vitro data on vesicle uptake and downstream cellular effects in colonic epithelial cultures.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 14
Figure 14 Diagram

Comprehensive mechanistic model summarizing how C. butyricum and its extracellular vesicles modulate gut homeostasis. This figure integrates findings on barrier function, immune modulation, and microbiome changes in experimental colitis.

Clostridium butyricum and Its Derived Extracellular Vesicles Modulate Gut Homeostasis and Ameliorate …

Figure 1. Outline of the pathways of synthesis for the n-3 and n-6 polyunsaturated fatty acids eicosanoids and the specialised pro-resolving mediators. AA, arachidonic acid; ALA, α-linolenic acid; COX, cyclooxygenase; CYTP450, cytochrome P450 enzymes; DHA
Figure 5 Diagram

N-3 and n-6 polyunsaturated fatty acids follow distinct biosynthetic pathways to produce eicosanoids and specialized pro-resolving mediators. This diagram outlines the synthesis routes from alpha-linolenic acid and arachidonic acid through COX and cytochrome P450 enzymes to their bioactive lipid products.

The Imbalance between n-6/n-3 Polyunsaturated Fatty Acids and Inflammatory Bowel Disease: A …

Figure 2. The n-3 polyunsaturated fatty acid targets of intestinal innate immunity. ALA, α-linolenic acid; CARD, caspase recognition domain; COX, cyclooxygenase; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; GPR, G-protein coupled receptor; ICAM,
Figure 6 Diagram

N-3 polyunsaturated fatty acids modulate intestinal innate immunity through multiple receptor and signaling targets. This diagram maps the interactions of DHA and EPA with G-protein coupled receptors, COX enzymes, and caspase recognition domains in intestinal immune cells.

The Imbalance between n-6/n-3 Polyunsaturated Fatty Acids and Inflammatory Bowel Disease: A …

Figure 3. The immuno-suppressive and immuno-resolving approaches of inflammatory bowel disease treatment. AZA, azathioprine; PUFA, polyunsaturated fatty acid; TNF, tumour necrosis factor.
Figure 7 Diagram

Current IBD treatments employ both immuno-suppressive and immuno-resolving strategies. This diagram contrasts conventional therapies (azathioprine, anti-TNF agents) with emerging PUFA-based approaches that promote active resolution of intestinal inflammation.

The Imbalance between n-6/n-3 Polyunsaturated Fatty Acids and Inflammatory Bowel Disease: A …

Figure 1
Figure 1 Flowchart

A double-blinded randomized placebo trial evaluated dietary fiber and probiotic formulas for functional constipation. This figure presents the study design, participant flow, or clinical outcomes showing how fiber and probiotic interventions modulated constipation symptoms and gut microbiota.

Effects of dietary fibers or probiotics on functional constipation symptoms and roles …

Figure 2
Figure 2 Chart

Gut microbiota composition changes were associated with symptom improvement in constipated patients receiving fiber or probiotic supplementation. This figure presents microbiome analysis data identifying bacterial taxa of relevance to constipation relief.

Effects of dietary fibers or probiotics on functional constipation symptoms and roles …

Figure 1. Immunomodulation by natural product compounds involves an altered balance between subsets of diverse immune cell types. The corresponding pathogenic (pro-inflammatory) (Right panel) versus protective (anti-inflammatory/immunomodulatory) (Left pane
Figure 6 Diagram

Natural product compounds shift the balance between pathogenic pro-inflammatory immune cells (right panel) and protective anti-inflammatory/immunomodulatory cell subsets (left panel). This diagram illustrates how diverse natural products can rebalance immune cell populations in autoimmune disease.

The Anti-Inflammatory and Immunomodulatory Activities of Natural Products to Control Autoimmune Inflammation.

Figure 7
Figure 7 Chart

In vivo models of autoimmune diseases have demonstrated therapeutic efficacy of various natural compounds. This figure presents preclinical evidence from animal models of rheumatoid arthritis, multiple sclerosis, or inflammatory bowel disease treated with natural products.

The Anti-Inflammatory and Immunomodulatory Activities of Natural Products to Control Autoimmune Inflammation.

Figure 8
Figure 8 Diagram

Clinical translation of natural anti-inflammatory products requires understanding of bioavailability and dose-response relationships. This figure discusses the therapeutic potential and limitations of natural product-based interventions for autoimmune conditions.

The Anti-Inflammatory and Immunomodulatory Activities of Natural Products to Control Autoimmune Inflammation.

Figure 1. Schematic of TLR4/NF-κB/AP-1 signaling.
Figure 5 Diagram

TLR4/NF-kB/AP-1 signaling is a key inflammatory pathway in intestinal disease. This schematic illustrates the cascade from TLR4 receptor activation through NF-kB and AP-1 transcription factors to pro-inflammatory gene expression, and indicates where curcumin may intervene.

Curcumin and Intestinal Inflammatory Diseases: Molecular Mechanisms of Protection.

Figure 2. (Reprinted with permission from Dove Medical Press, Ltd.). Effect of FLLL32 and curcumin on IL-6-induced reduction of TEER in T84 monolayer. TEER value of T84 monolayers incubated with cell culture medium for 0–72 h in the presence of IL-6 (10 ng
Figure 6 Chart

FLLL32 (a curcumin analogue) and curcumin both protect against IL-6-induced reduction of transepithelial electrical resistance (TEER) in T84 cell monolayers. This graph shows that curcumin preserves intestinal barrier integrity by counteracting cytokine-mediated tight junction disruption over 72 hours.

Curcumin and Intestinal Inflammatory Diseases: Molecular Mechanisms of Protection.

Figure 7
Figure 7 Chart

Curcumin's effects on intestinal tight junction proteins have been demonstrated in multiple experimental models. This figure presents protein expression or immunofluorescence data showing curcumin-mediated preservation of barrier function.

Curcumin and Intestinal Inflammatory Diseases: Molecular Mechanisms of Protection.

Figure 8
Figure 8 Chart

Animal models of necrotizing enterocolitis and colitis respond favorably to curcumin treatment. This figure presents in vivo data on curcumin's protective effects in experimental intestinal inflammation.

Curcumin and Intestinal Inflammatory Diseases: Molecular Mechanisms of Protection.

Figure 1. Inflammatory bowel diseases (IBD), activation of the nuclear factor-kB (NF-kB), and the possible roles of phytochemicals against this pathway activation during these diseases. ↑, increase; TLRs, Toll-like receptors; IKKα, IkappaB kinase alfa; IKK
Figure 6 Diagram

Inflammatory bowel diseases are associated with activation of the NF-kB signaling pathway. This diagram illustrates how various phytochemicals may counteract NF-kB pathway activation through inhibition of Toll-like receptors, IKK complex, and downstream transcriptional targets in IBD.

Phytochemicals and Regulation of NF-kB in Inflammatory Bowel Diseases: An Overview of …

Figure 218
Figure 218 Diagram

Supplementary figure from a comprehensive review of phytochemical effects on NF-kB regulation in inflammatory bowel disease. The review examines multiple plant-derived compounds with potential to attenuate chronic intestinal inflammation through modulation of key signaling pathways.

Phytochemicals and Regulation of NF-kB in Inflammatory Bowel Diseases: An Overview of …

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