Berberine represses Wnt/β-catenin pathway activation via modulating the microRNA-103a-3p/Bromodomain-containing protein 4 axis, thereby refraining pyroptosis and reducing the intestinal mucosal barrier defect induced via colitis

Zhao, Xun; Cui, Dejun; Yuan, W B; Chen, Chen; Liu, Qi

doi:10.1080/21655979.2022.2047405

Cited by 13 publications

(9 citation statements)

References 53 publications

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“…Polyphenols, found mainly in fruits and vegetables, are complex molecules produced by plants with antioxidant properties able to scavenge free radicals. Divided into flavonoids (such as alpinetin, fortunellin, baicalin, quercetin, berberine, cardamonin and lonicerin) [ 168 , 169 , 170 , 171 , 172 , 173 , 174 ] and non-flavonoids (such as resveratrol [ 175 , 176 ] and chlorogenic acid [ 177 ]), they reduce the risk of intestinal inflammation, mainly by modifying the miRs profile and inhibiting HDACs. Other foods have also been shown to influence host epigenetics and could potentially play a role in gut inflammation.…”

Section: Resultsmentioning

confidence: 99%

Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models

Vieujean

Caron

Haghnejad

et al. 2022

IJMS

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Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the gastrointestinal tract that encompass two main phenotypes, namely Crohn’s disease and ulcerative colitis. These conditions occur in genetically predisposed individuals in response to environmental factors. Epigenetics, acting by DNA methylation, post-translational histones modifications or by non-coding RNAs, could explain how the exposome (or all environmental influences over the life course, from conception to death) could influence the gene expression to contribute to intestinal inflammation. We performed a scoping search using Medline to identify all the elements of the exposome that may play a role in intestinal inflammation through epigenetic modifications, as well as the underlying mechanisms. The environmental factors epigenetically influencing the occurrence of intestinal inflammation are the maternal lifestyle (mainly diet, the occurrence of infection during pregnancy and smoking); breastfeeding; microbiota; diet (including a low-fiber diet, high-fat diet and deficiency in micronutrients); smoking habits[ vitamin D and drugs (e.g., IBD treatments, antibiotics and probiotics). Influenced by both microbiota and diet, short-chain fatty acids are gut microbiota-derived metabolites resulting from the anaerobic fermentation of non-digestible dietary fibers, playing an epigenetically mediated role in the integrity of the epithelial barrier and in the defense against invading microorganisms. Although the impact of some environmental factors has been identified, the exposome-induced epimutations in IBD remain a largely underexplored field. How these environmental exposures induce epigenetic modifications (in terms of duration, frequency and the timing at which they occur) and how other environmental factors associated with IBD modulate epigenetics deserve to be further investigated.

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Section: Resultsmentioning

confidence: 99%

Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models

Vieujean

Caron

Haghnejad

et al. 2022

IJMS

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“…Several compounds can modulate pyroptosis in intestinal injury. Berberine inhibits Wnt/b-catenin pathway activation by modulating the miR-103a-3p-BRD4 axis, inhibits pyroptosis, and reduces the intestinal mucosal barrier defects caused by colitis [148]. Schisandrin B reduces ROS-induced mitochondrial damage by inhibiting pyroptosis and epithelial cell damage in colitis [149].…”

Section: Pyroptosis and Intestinal Injurymentioning

confidence: 99%

The Induction Mechanism of Ferroptosis, Necroptosis, and Pyroptosis in Inflammatory Bowel Disease, Colorectal Cancer, and Intestinal Injury

et al. 2023

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Cell death includes programmed and nonprogrammed cell death. The former mainly includes ferroptosis, necroptosis, pyroptosis, autophagy, and apoptosis, while the latter refers to necrosis. Accumulating evidence shows that ferroptosis, necroptosis, and pyroptosis play essential regulatory roles in the development of intestinal diseases. In recent years, the incidence of inflammatory bowel disease (IBD), colorectal cancer (CRC), and intestinal injury induced by intestinal ischemia–reperfusion (I/R), sepsis, and radiation have gradually increased, posing a significant threat to human health. The advancement in targeted therapies for intestinal diseases based on ferroptosis, necroptosis, and pyroptosis provides new strategies for treating intestinal diseases. Herein, we review ferroptosis, necroptosis, and pyroptosis with respect to intestinal disease regulation and highlight the underlying molecular mechanisms for potential therapeutic applications.

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“…Therefore, Brd4 appears to modulate the activation of different forms of inflammasome in response to distinct stimuli and the detailed molecular mechanisms merit further investigation (Fig. 4) [15,110,112,[116][117][118][119].…”

Section: Brd4 and Pyroptosismentioning

confidence: 99%

Regulation of programmed cell death by Brd4

Pan

et al. 2022

Cell Death Dis

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Epigenetic factor Brd4 has emerged as a key regulator of cancer cell proliferation. Targeted inhibition of Brd4 suppresses growth and induces apoptosis of various cancer cells. In addition to apoptosis, Brd4 has also been shown to regulate several other forms of programmed cell death (PCD), including autophagy, necroptosis, pyroptosis, and ferroptosis, with different biological outcomes. PCD plays key roles in development and tissue homeostasis by eliminating unnecessary or detrimental cells. Dysregulation of PCD is associated with various human diseases, including cancer, neurodegenerative and infectious diseases. In this review, we discussed some recent findings on how Brd4 actively regulates different forms of PCD and the therapeutic potentials of targeting Brd4 in PCD-related human diseases. A better understanding of PCD regulation would provide not only new insights into pathophysiological functions of PCD but also provide new avenues for therapy by targeting Brd4-regulated PCD.

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Berberine represses Wnt/β-catenin pathway activation via modulating the microRNA-103a-3p/Bromodomain-containing protein 4 axis, thereby refraining pyroptosis and reducing the intestinal mucosal barrier defect induced via colitis

Cited by 13 publications

References 53 publications

Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models

Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models

The Induction Mechanism of Ferroptosis, Necroptosis, and Pyroptosis in Inflammatory Bowel Disease, Colorectal Cancer, and Intestinal Injury

Regulation of programmed cell death by Brd4

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