Changes in serum inflammatory cytokine levels and intestinal flora in a self-healing dextran sodium sulfate-induced ulcerative colitis murine model

Jialing, Liu; Gao, Yangyang; Zhou, Jing; Tang, Xin; Wang, Ping; Shen, Liwei; Chen, Simin

doi:10.1016/j.lfs.2020.118587

Cited by 69 publications

(48 citation statements)

References 44 publications

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“…Hyperactivation macrophages were closely linked to the onset and recurrence of mucosal in ammation in UC. Increasing evidence suggests that targeted regulation of macrophage activation is an emerging strategy for UC treatment [23]. In this study, the percentage of CD11b + F4/80 + (Fig.…”

Section: Ginsenoside Rg1 Inhibited Macrophage Activationmentioning

confidence: 60%

“…Alpha diversity analysis reveals intestinal ora imbalance in IBD patients with higher abundance of harmful bacteria such as E. coli, Shigella and gamma-amoeba, and lower abundance of bene cial bacteria Lactobacillus, Bi dobacterium and Phytophthora [40,41]. In colitis model, the composition and relative abundance of intestinal ora present signi cant changes, with lower abundance of Bacteroidales_S24-7_group_unidenti ed, Bacteroides Prevotellaceae_UCG-001, Lactobacillus and Alistipes, and higher abundance of Streptococcus and Shigella [23,42]. Not entirely consistent with these studies, we found that the relative abundance of Lachnospiraceae_NK4A136_group, unclassi ed_f_Lachnospiraceae and norank_f_Lachnospiraceae were signi cantly decreased, and that of Staphylococcus, Bacteroides, Prevotelaceae_UCG-001 and Eubacterium_ ssicatena_group were signi cantly increased.…”

Section: Discussionmentioning

confidence: 99%

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Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

Long

Liu

Kang

et al. 2021

Preprint

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Background: Aberrant M1/M2 macrophage polarization and intestinal flora disruption are involved in the pathological processes associated with ulcerative colitis (UC). Ginsenoside Rg1 has good immunomodulatory and anti-inflammatory effects and is effective in treating UC of humans and animals. However, it is unclear how ginsenoside Rg1 regulate the homeostasis of M1/M2 macrophage polarization and intestinal flora.Methods: BALB/c mice were randomly divided into 4 groups: Control, DSS, DSS+Rg1, DSS+Y27632 groups. In this study, experiment colitis was induced in BALB/c mice using sodium dextran sulfate (DSS). Mice of DSS+Rg1, DSS+Y27632 groups were treated respectively with ginsenoside Rg1 and Rock inhibitor Y27632 for 14 consecutive days. On day 21, all mice were sacrificed. Histopathological analysis of the colon tissues was performed by Hematoxylin Eosin sinning. Cytokines (IL-6, IL-33, CCL-2, TNF-α, IL-4 and IL-10) were detected by Elisa. Flow cytometry was used to analyse macrophage activation and M1/M2 macrophage polarisation. Western blotting were applied to detect the levels of Macrophage polarization-associated protein (Arg-1, MIF-1, PIM-1, TLR2) and Nogo-B/RhoA signaling molecules (Rock1, RhoA and Nogo-B). The fecal microbial populations were analyzed using 16S gene sequencing. Results: After ginsenoside Rg1 and Y27632 treatment, the changes of body weight, colon length, colonic weight index and colonic mucosal injury of colitis mice were effectively improved, accompanied by less ulcer formation and inflammatory cell infiltration, lower levels of pro-inflammatory cytokines (IL-6, IL-33, CCL-2, TNF-α) and higher anti-inflammatory cytokines (IL-4 and IL-10). Importantly, the percentage of CD11b+F4/80+, CD11b+F4/80+Tim-1+, CD11b+F4/80+TLR4+, and CD11b+F4/80+iNOS+ cells and the expression levels of MIF-1 and PIM-1 proteins were down-regulated significantly after ginsenoside Rg1 and Y27632 treatment, and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ cells and Arg-1 up-regulated significantly. Intestinal flora composition were effectively improved after administration of ginsenoside Rg1. The Nogo-B/RchoA signaling pathway were obviously inhibited after ginsenoside Rg1 and Y27632 treatment, and the levels of Rock1, RhoA and Nogo-B proteins were significantly reduced. Conclusions: Ginsenoside Rg1 has the protective effect on UC by inhibiting macrophage activation, restoring the balance of M1/M2 macrophage polarization, and improving intestinal flora composition, associated with inhibition of the Nogo-B/RhoA signaling pathway.

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Section: Ginsenoside Rg1 Inhibited Macrophage Activationmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

Long

Liu

Kang

et al. 2021

Preprint

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“…The activation of B cells in peripheral blood has been reported to be specific to CD patients rather than UC patients, and IL-8 secreted by B cells is one of the causes of aggravation of CD. [45] In contrast, there is no significant upregulation of IL-8 in peripheral blood and colonic localization but upregulation of IL-10 in colonic localization, which indicates that the B cells that responded in the DSS group of mice may be regulatory B cells. Regulatory B cells can secrete IL-10 to regulate inflammatory activities.…”

Section: Discussionmentioning

confidence: 88%

“…DSS-induced damage in the intestinal barrier further allowed the entry of bacteria and antigens from the intestinal lumen into the intestinal mucosal layer, causing local inflammation throughout the intestinal wall, which was in line with the lesions in human patients with fulminant or severe UC. [5,6,17] The TNBS induced epithelial damage in the mucosal layer, accompanied by loss of necrotic cell and partial crypt damage. A small amount of inflammatory cell infiltration was seen in the lamina propria, manifesting as mucosal erosion and localized congestion in the lamina propria, which is inseparable from the cascade immune response caused by TNBS.…”

Section: Discussionmentioning

confidence: 99%

“…In order to assess the effects of DSS and TNBS modeling, the body weights of mice were evaluated: As shown in Figure 1, the disease activity in the DSS group mice increased within 7 days, which was consistent with the studies by Jialing L et. [17] . Different from DSS-treated mice, the TNBS-treated mice had more obvious and severe symptoms in diarrhea and loose stools at the first three days of modeling with less blood in the feces, which gradually subsided afterward.…”

Section: Differences In Ordinary Circumstances and Dai Scores Between The Dss And Tnbs Modelsmentioning

confidence: 99%

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Different Mechanism and Efficacy of Dextran-Sodium Sulfate and 2,4,6-Trinitrobenzene Sulphonic Acid in Modeling Ulcerative Colitis in C57BL/6 Mice

et al. 2021

Preprint

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Background and Aims: Dextran-sodium sulfate and 2,4,6-trinitrobenzene sulphonic acid are common modeling methods in studying ulcerative colitis. Little attention has been paid to the mechanism differences between the two approaches. Here, we aim to compare the mechanisms and efficacy of these two models and wish to provide fundamental proves for choosing ideal ulcerative colitis models. Methods: Dextran-sodium sulfate and 2,4,6-trinitrobenzene sulphonic acid were applied to induce the colitis in C57BL/6 mice for seven days. Body weight and disease activity index were assessed. Hematology was detected by routine blood test. Histopathology was analyzed by hematoxylin-eosin staining section. Enzyme-linked immunosorbent assay, Western blot and quantitative real-time PCR were used to detect the cytokines protein levels and mRNA levels. Flow cytometry were used to detect the cycles and subsets of splenic cells. Results: Dextran-sodium sulfate induced colitis in C57BL/6 mice showed higher acute immune activities, while 2,4,6-trinitrobenzene sulphonic acid induced colitis showed chronic immune activities with high platelet amounts and activation. Dextran-sodium sulfate is more suitable for modeling acute ulcerative colitis. On the contrary, 2,4,6-trinitrobenzene sulphonic acid is more appropriate for modeling chronic ulcerative colitis. Conclusions: Dextran-sodium sulfate treatment within 7 days in C57BL/6 mice is a suitable experimental model for studying human acute ulcerative colitis with immune response, fecal blood and acute pathogenic damage. Conversely, 2,4,6-trinitrobenzene sulphonic acid treatment within 7 days is more appropriate for studying human chronic ulcerative colitis with hypercoagulable state, IL-2 over-expression state and chronic pathogenic damage.

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Lacticaseibacillus casei ATCC334 Ameliorates Radiation‐Induced Intestinal Injury in Rats by Targeting Microbes and Metabolites

Hua

Zhang

Xu³

et al. 2022

Molecular Nutrition Food Res

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Scope Gastrointestinal side effects are frequently observed in patients receiving medical radiation therapy. As Lacticaseibacillus casei ATCC334 potentially affects microbial ecosystem, the study hypothesizes that it may improve radiation‐induced intestinal injury in rats by modulating the “gut microbiota‐metabolite‐barrier axis.” Methods and results Rats are fed one of three or no doses of L. casei ATCC334 for 7 days and then expose to a single dose of 9 Gy X‐ray total abdominal irradiation. Supplementation with L. casei ATCC334 promote the proliferation of intestinal stem cells (ISCs), increase the expression of tight junction proteins, reduce intestinal permeability, and protect intestinal barrier integrity. Moreover, 16S rRNA sequencing show that medium and high doses of L. casei ATCC334 inhibit the growth of Escherichia/Shigella and favor Akkermansia proliferation. L. casei ATCC334 intervention reprogram the metabolic profile and inhibit putrescine production but promote alpha‐linolenic acid (ALA) production. Notably, a decrease in putrescine and an increase in ALA are significantly correlated with the proliferation of ISCs and enhanced intestinal barrier function following L. casei ATCC334 intervention. Conclusion These results highlight that medium and high doses of L. casei ATCC334 alleviate radiation‐induced intestinal damage by enhancing the mucosal barrier and remodeling the gut microbiota structure and metabolic activity.

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Changes in serum inflammatory cytokine levels and intestinal flora in a self-healing dextran sodium sulfate-induced ulcerative colitis murine model

Cited by 69 publications

References 44 publications

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

Ginsenoside Rg1 Ameliorated Colitis by Regulating the Homeostasis of M1/M2 Macrophage Polarization and Intestinal Flora

Different Mechanism and Efficacy of Dextran-Sodium Sulfate and 2,4,6-Trinitrobenzene Sulphonic Acid in Modeling Ulcerative Colitis in C57BL/6 Mice

Lacticaseibacillus casei ATCC334 Ameliorates Radiation‐Induced Intestinal Injury in Rats by Targeting Microbes and Metabolites

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