Modulation of Gut Microbiota Combined with Upregulation of Intestinal Tight Junction Explains Anti-Inflammatory Effect of Corylin on Colitis-Associated Cancer in Mice

Chang, Zi‐Yu; Liu, Hsuan-Miao; Leu, Yann Lii; Hsu, Cheng Hsiung; Lee, Tzung-Yan

doi:10.3390/ijms23052667

Cited by 39 publications

(27 citation statements)

References 66 publications

(73 reference statements)

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“…Intestinal epithelial cells (IECs) formed various kinds of mucosal layers separating gut microbes and immune cells to prevent the following overreaction of inflammation, which can be viewed as a critical barrier to intestinal homeostasis. It has been proven that dysbiosis is associated with intestinal inflammation in animal models of colitis [ 43 ]. Still, studies have also found that both declines of tight junction proteins (like ZO-1, claudin-1, occludin) and increasing permeability (leaky gut) appear forward to severe gut inflammation.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Gut Microbiota and Upregulations of VPAC2 and Intestinal Tight Junctions Correlate with Anti-Inflammatory Effects of Electroacupuncture in Colitis Mice with Sleep Fragmentation

Liu

Zhuo

Huang

et al. 2022

Biology

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The relationship between inflammatory bowel disease and sleep disturbances is complicated and of increasing interest. We investigated the inflammatory and immunological consequences of EA in sleep-deprived colitis and found that dextran sulfate sodium (DSS)-induced colitis in sleep-fragmented (SF) mice was more severe than that in mice with normal sleep. This increase in the severity of colitis was accompanied by reduced body weight, shortened colon length, and deteriorated disease activity index. DSS with SF mice presented obvious diminished intestinal tight junction proteins (claudin-1 and occludin), elevated proinflammatory cytokines (CRP, IFN-γ, IL-6), lowered melatonin and adiponectin levels, downregulated vasoactive intestinal peptide (VIP) type 1 and 2 receptor (VPAC1, VPAC2) expression, and decreased diversity of gut bacteria. EA ameliorated colitis severity and preserved the performance of the epithelial tight junction proteins and VIP receptors, especially VPAC2. Meanwhile, the innate lymphoid cells-derived cytokines in both group 2 (IL-4, IL5, IL-9, IL-13) and group 3 (IL-22, GM-CSF) were elevated in mice colon tissue. Furthermore, dysbiosis was confirmed in the DSS group with and without SF, and EA could maintain the species diversity. Firmicutes could be restored, such as Lachnospiraceae, and Proteobacteria become rebalanced, mainly Enterobacteriaceae, after EA intervention. On the other hand, SF plays different roles in physiological and pathological conditions. In normal mice, interrupted sleep did not affect the expression of claudin-1 and occludin. But VPAC1, VPAC2, and gut microbiota diversity, including Burkholderiaceae and Rhodococcus, were opposite to mice in an inflamed state.

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Section: Discussionmentioning

confidence: 99%

Alterations in Gut Microbiota and Upregulations of VPAC2 and Intestinal Tight Junctions Correlate with Anti-Inflammatory Effects of Electroacupuncture in Colitis Mice with Sleep Fragmentation

Liu

Zhuo

Huang

et al. 2022

Biology

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“…The role of Romboutsia in gut inflammation remains unclear. In some studies, Romboutsia was considered as beneficial bacteria in acute colitis [ 75 ], but its enrichment was in DSS-induced chronic colitis [ 76 , 77 ] and azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) [ 78 ]. Consistent with an aforementioned study [ 78 ], our results showed that DSS could increase Romboutsia abundance.…”

Section: Discussionmentioning

confidence: 99%

“…In some studies, Romboutsia was considered as beneficial bacteria in acute colitis [ 75 ], but its enrichment was in DSS-induced chronic colitis [ 76 , 77 ] and azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) [ 78 ]. Consistent with an aforementioned study [ 78 ], our results showed that DSS could increase Romboutsia abundance. Klebsiella , a pathogen belonging to the family Enterobacteriaceae , was significantly more abundant in the gut of mice with DSS-induced colitis [ 79 , 80 ] and played a key role in pathological damage initiation and perpetuation in various intestinal inflammations and cancers [ 57 , 81 , 82 ].…”

Section: Discussionmentioning

confidence: 99%

Alginate Oligosaccharides Ameliorate DSS-Induced Colitis through Modulation of AMPK/NF-κB Pathway and Intestinal Microbiota

Zhang

Guo

et al. 2022

Nutrients

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Alginate oligosaccharides (AOS) are shown to have various biological activities of great value to medicine, food, and agriculture. However, little information is available about their beneficial effects and mechanisms on ulcerative colitis. In this study, AOS with a polymerization degree between 2 and 4 were found to possess anti-inflammatory effects in vitro and in vivo. AOS could decrease the levels of nitric oxide (NO), IL-1β, IL-6, and TNFα, and upregulate the levels of IL-10 in both RAW 264.7 and bone-marrow-derived macrophage (BMDM) cells under lipopolysaccharide (LPS) stimulation. Additionally, oral AOS administration could significantly prevent bodyweight loss, colonic shortening, and rectal bleeding in dextran sodium sulfate (DSS)-induced colitis mice. AOS pretreatment could also reduce disease activity index scores and histopathologic scores and downregulate proinflammatory cytokine levels. Importantly, AOS administration could reverse DSS-induced AMPK deactivation and NF-κB activation in colonic tissues, as evidenced by enhanced AMPK phosphorylation and p65 phosphorylation inhibition. AOS could also upregulate AMPK phosphorylation and inhibit NF-κB activation in vitro. Moreover, 16S rRNA gene sequencing of gut microbiota indicated that supplemental doses of AOS could affect overall gut microbiota structure to a varying extent and specifically change the abundance of some bacteria. Medium-dose AOS could be superior to low- or high-dose AOS in maintaining remission in DSS-induced colitis mice. In conclusion, AOS can play a protective role in colitis through modulation of gut microbiota and the AMPK/NF-kB pathway.

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“…However, there are no reports about the relationship between Patescibacteria and PD. Patescibacteria is an interesting but currently not widely understood anaerobic bacterium [ 33 ]. In the cerebral cortex and hippocampus of a rat model of chronic unpredictable mild stress (CUMS), Zhang et al found that it was positively associated with 5-hydroxy tryptamine (5-HT), brain-derived neurotrophic factor (BDNF), and glucagon-likepeptide-1 (GLP-1) [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Curcumin Regulates Gut Microbiota and Exerts a Neuroprotective Effect in the MPTP Model of Parkinson’s Disease

Zhu

Zhang

Hou

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objectives. The experiment aimed to explore the effects of curcumin on motor impairment, dopamine neurons, and gut microbiota in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mice model. Methods. Mice were randomly assigned to six groups: normal control group, solvent control group, MPTP group, curcumin-low-dose group (40 mg/kg), curcumin-medium-dose group (80 mg/kg), and curcumin-high-dose group (160 mg/kg). After 14 days, each group of mice was subjected to the pole text, the hanging test, and the open-field test. Tyrosine hydroxylase (TH) immunohistochemistry was used to observe the survival of nigrostriatal dopamine neurons. Moreover, ultrastructural changes were observed with a transmission electron microscope in mice striatal tissue cells. Then, 16S rRNA was used to assess changes in the gut microbiota. Results. (1) Each dose of curcumin reduced pole climbing time and increased suspension score and total distance moved dose-dependently. (2) All curcumin groups improved cell wrinkling and vacuolar degeneration, increased the number of TH positives, improved cell survival, and the higher the dose of curcumin, the better the effect. (3) There were differences in microbiota composition and a relative abundance among the groups. The relative abundance of Patescibacteria, Proteobacteria, and Verrucomicrobia was higher in the MPTP group. The relative abundance of Patescibacteria, Enterobacteriaceae, Enterococcaceae all decreased in all curcumin groups. In addition, the Kyoto Encyclopedia of Genes and Genomes pathways showed a reduction in the superpathway of N-acetylneuraminate degradation after medium- and high-dose curcumin administration. Conclusions. Curcumin regulates gut microbiota and exerts a neuroprotective effect in the MPTP mice model. This preliminary study demonstrates the therapeutic potential of curcumin for Parkinson’s disease, providing clues for microbially targeted therapies for Parkinson’s disease.

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Modulation of Gut Microbiota Combined with Upregulation of Intestinal Tight Junction Explains Anti-Inflammatory Effect of Corylin on Colitis-Associated Cancer in Mice

Cited by 39 publications

References 66 publications

Alterations in Gut Microbiota and Upregulations of VPAC2 and Intestinal Tight Junctions Correlate with Anti-Inflammatory Effects of Electroacupuncture in Colitis Mice with Sleep Fragmentation

Alterations in Gut Microbiota and Upregulations of VPAC2 and Intestinal Tight Junctions Correlate with Anti-Inflammatory Effects of Electroacupuncture in Colitis Mice with Sleep Fragmentation

Alginate Oligosaccharides Ameliorate DSS-Induced Colitis through Modulation of AMPK/NF-κB Pathway and Intestinal Microbiota

Curcumin Regulates Gut Microbiota and Exerts a Neuroprotective Effect in the MPTP Model of Parkinson’s Disease

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