Emodin Protects Sepsis Associated Damage to the Intestinal Mucosal Barrier Through the VDR/ Nrf2 /HO-1 Pathway

Shang, Luorui; Liu, Yuhan; Li, Jinxiao; Pan, Guangtao; Zhou, Fangyuan; Yang, Shenglan

doi:10.3389/fphar.2021.724511

Cited by 23 publications

(14 citation statements)

References 46 publications

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“… 143 Emodin from Polygonum multiflorum can also protect the colonic mucosal barrier through increases in the mRNA and protein expression of the VDR and its downstream molecules, Nrf2 and HO‐1. 144 Although these experiments demonstrate the protective effect of emodin, Cheng et al have found that its long‐term administration produces toxic metabolites, because colon microorganisms convert rhubarb anthraquinones to rhein, which accumulates over time and causes melanosis coli to increase the risk of colon cancer. 145 Shao et al indicated that Sophora flavescens Aiton EtOAc extract (SFE) inhibits oxidative stress and immune inflammation in UC mice, mainly manifested as linoleic acid, arachidonic acid, and fatty acid metabolism recovery, and reduces the expression of related inflammatory markers.…”

Section: Regulation Of the Intestinal Microbiota To Treat Ibdmentioning

confidence: 99%

“…In the experimental UC model, KD, through regulating the intestinal microbiota and reducing the level of TLR‐dependent phosphorylated PI3K/AKT/NF‐κB, protected the colonic mucosa 143 . Emodin from Polygonum multiflorum can also protect the colonic mucosal barrier through increases in the mRNA and protein expression of the VDR and its downstream molecules, Nrf2 and HO‐1 144 . Although these experiments demonstrate the protective effect of emodin, Cheng et al have found that its long‐term administration produces toxic metabolites, because colon microorganisms convert rhubarb anthraquinones to rhein, which accumulates over time and causes melanosis coli to increase the risk of colon cancer 145 .…”

Section: Regulation Of the Intestinal Microbiota To Treat Ibdmentioning

confidence: 99%

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Research progress on the relationship between intestinal microecology and intestinal bowel disease

Song

et al. 2022

Anim Models and Exp Med

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Intestinal microecology is the main component of human microecology. Intestinal microecology consists of intestinal microbiota, intestinal epithelial cells, and intestinal mucosal immune system. These components are interdependent and establish a complex interaction network that restricts each other. According to the impact on the human body, there are three categories of symbiotic bacteria, opportunistic pathogens, and pathogenic bacteria. The intestinal microecology participates in digestion and absorption, and material metabolism, and inhibits the growth of pathogenic microorganisms. It also acts as the body's natural immune barrier, regulates the innate immunity of the intestine, controls the mucosal barrier function, and also participates in the intestinal epithelial cells' physiological activities such as hyperplasia or apoptosis. When the steady-state balance of the intestinal microecology is disturbed, the existing core intestinal microbiota network changes and leads to obesity, diabetes, and many other diseases, especially irritable bowel syndrome, inflammatory bowel disease (IBD), and colorectal malignancy. Intestinal diseases, including tumors, are particularly closely related to intestinal microecology. This article systematically discusses the research progress on the relationship between IBD and intestinal microecology from the pathogenesis, treatment methods of IBD, and the changes in intestinal microbiota.

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Section: Regulation Of the Intestinal Microbiota To Treat Ibdmentioning

confidence: 99%

Section: Regulation Of the Intestinal Microbiota To Treat Ibdmentioning

confidence: 99%

Research progress on the relationship between intestinal microecology and intestinal bowel disease

Song

et al. 2022

Anim Models and Exp Med

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“…CYC can damage intestinal epithelial cells, resulting in increased intestinal permeability, impaired intestinal mucosal oxidation, and intestinal microbiota disorder, thus damaging intestinal immune function [ 30 , 31 ]. SOD activity can indirectly reflect the ability of scavenging oxygen free radicals, and MDA can be used to judge the level of oxygen free radicals in the colonic mucosa, the intensity of lipid peroxidation, and the degree of tissue damage [ 32 ]. Cai et al [ 33 ] found that alhagi honey polysaccharides significantly improve intestinal SOD activity, reduce MDA content, relieve intestinal oxidative stress injury, and the protect intestinal barrier in CYC mice.…”

Section: Discussionmentioning

confidence: 99%

Preventive Mechanism of Lycopene on Intestinal Toxicity Caused by Cyclophosphamide Chemotherapy in Mice by Regulating TLR4-MyD88/TRIF-TRAF6 Signaling Pathway and Gut-Liver Axis

Xiao

Niu

et al. 2022

Nutrients

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Cyclophosphamide (CYC) is the first-line chemotherapy drug for cancer in clinical practice, and its intestinal toxicity seriously affects the treatment effect and prognosis of patients. Lycopene (LP) is the main pigment of ripe tomatoes and has strong antioxidant activity. However, the mechanism by which LP prevents CYC-induced intestinal injury remains unclear. The aim of this study was to investigate the mechanism of LP in preventing intestinal toxicity caused by CYC chemotherapy in mice. The results showed that LP significantly prevented spleen and thymus atrophy induced by CYC. In terms of intestinal injury, LP significantly increased the levels of superoxide dismutase (SOD), secretory immunoglobulin A (sIgA), interleukin (IL)-4, IL-12, and interferon (IFN)-γ, decreased the content of lipid oxidation (MDA), upregulated the protein expressions of toll-like receptors 4 (TLR4), myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor-associated factor 6 (TRAF6), toll/IL-1receptor domain containing adaptor protein inducing IFN-β (TRIF), p-P38 MAPK (P38), and p- nuclear factor kappa-B (NF-κB) p65, and improved the small intestine tissue injury induced by CYC. In terms of liver injury, LP significantly increased the content of glutathione (GSH), decreased the contents of MDA, nitric oxide (NO), IL-1β, IL-6, and tumor necrosis factor (TNF)-α, and repaired the liver tissue injury induced by CYC. Importantly, 10 mg/kg LP significantly prevented intestinal microbiota dysregulation in CYC mice. These results suggested that LP significantly prevented intestinal injury induced by CYC in mice by regulating the TLR4-MyD88/TRIF-TRAF6 signaling pathway and gut-liver axis.

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“…NCM460 human colonic epithelial cells were purchased from Shanghai Meiwan Biotechnology Co., Ltd and grown in RPMI medium containing penicillin (100 U/ml)-streptomycin (100 U/ml) (Invitrogen, Carlsbad, CA, United States) and 10% fetal bovine serum (Hyclone, Logan, UT, United States) ( Zhou et al, 2018 ). Lipopolysaccharide (LPS, 10 ng/ml) was used to induce inflammation and autophagy in NCM460 cells ( Zeng et al, 2018 ; Ba et al, 2021 ; Guo et al, 2021 ; Shang et al, 2021 ). The groups were divided into control, LPS, LPS+HLD-DS, LPS+HLD-DS+3-MA, LPS+HLD-DS+RAPA, LPS+HLD-DS+PDTC, LPS+HLD-DS+PDTC+RAPA, and LPS+HLD-DS+PDTC+3-MA.…”

Section: Methodsmentioning

confidence: 99%

Huangkui lianchang decoction attenuates experimental colitis by inhibiting the NF-κB pathway and autophagy

Cheng

Zhou

et al. 2022

Front. Pharmacol.

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Ulcerative colitis (UC) is a chronic inflammatory colorectal disease characterized by excessive mucosal immune response activation and dysfunction of autophagy in intestinal epithelial cells. Traditional herbal preparations, including the Huangkui lianchang decoction (HLD), are effective in UC clinical treatment in East Asia, but the underlying mechanism is unclear. This study evaluated the therapeutic effects and associated molecular mechanisms of HLD in UC in vivo and in vitro. A C57BL/6 UC mouse model was established using 2.5% dextran sulfate sodium. The effects of HLD on the colonic structure and inflammation in mice were evaluated using mesalazine as the control. The anti-inflammatory effects of HLD were assessed using disease activity index (DAI) scores, histological scores, enzyme-linked immunosorbent assay, immunohistochemistry, immunofluorescence, and western blotting. HLD displayed a protective effect in UC mice by reducing the DAI and colonic histological scores, as well as levels of inflammatory cytokines and NF-κB p65 in colonic tissues. NCM460 lipopolysaccharide-induced cells were administered drug serum-containing HLD (HLD-DS) to evaluate the protective effect against UC and the effect on autophagy. HLD-DS exhibited anti-inflammatory effects in NCM460 cells by reducing the levels of inflammatory cytokines and increasing interleukin 10 levels. HLD-DS reduced p-NF-κB p65, LC3II/I, and Beclin 1 expression, which suggested that HLD alleviated colitis by inhibiting the NF-κB pathway and autophagy. However, there was no crosstalk between the NF-κB pathway and autophagy. These findings confirmed that HLD was an effective herbal preparation for the treatment of UC.

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Emodin Protects Sepsis Associated Damage to the Intestinal Mucosal Barrier Through the VDR/ Nrf2 /HO-1 Pathway

Cited by 23 publications

References 46 publications

Research progress on the relationship between intestinal microecology and intestinal bowel disease

Research progress on the relationship between intestinal microecology and intestinal bowel disease

Preventive Mechanism of Lycopene on Intestinal Toxicity Caused by Cyclophosphamide Chemotherapy in Mice by Regulating TLR4-MyD88/TRIF-TRAF6 Signaling Pathway and Gut-Liver Axis

Huangkui lianchang decoction attenuates experimental colitis by inhibiting the NF-κB pathway and autophagy

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