Dihydromyricetin Protects Intestinal Barrier Integrity by Promoting IL-22 Expression in ILC3s through the AMPK/SIRT3/STAT3 Signaling Pathway

Zhou, Jie; Yue, Jing; Yu, Yongguang; Hou, Pengfei; Zhang, Ting; Zhang, Qianyong; Lv, Yi; Mi, Mantian

doi:10.3390/nu15020355

Cited by 10 publications

(6 citation statements)

References 49 publications

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“…Melatonin attenuates sepsis-induced small-intestine injury by up-regulating Sirt3-mediated oxidative-stress inhibition, mitochondrial protection, and autophagy induction, ( 18 ) and moreover, dihydromyricetin protects intestinal barrier integrity through regulating Sirt3. ( 19 ) Our results indicate that Sirt3 plays an negative role in the development of colitis, and maybe an promising pharmacological target to facilitate specific medicine development.…”

Section: Discussionmentioning

confidence: 74%

Sirtuin 3 ameliorates inflammatory bowel disease via inhibiting intestinal inflammation and oxidative stress

Qin,

Chu,

Ding

et al. 2024

J. Clin. Biochem. Nutr.

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Sirtuin 3 involved in development of various diseases, but its role in inflammatory bowel disease is still unknown. We used inflammatory bowel disease biopsies, colitis animal model, and vitro cells RAW264.7 to study the role of Sirtuin 3 in the pathophysiology of inflammatory bowel disease. Sirtuin 3 negatively correlated with intestinal TNF-α. Sirt3 was less pronounced in pediatric and adult inflammatory bowel disease patients compared with corresponding control group. Sirtuin 3 activator Honokiol suppressed dextran sulfate sodium induced colonic manifestations, while Sirt3 inhibitor caused opposite results. Honokiol inhibited colonic oxidative stress by and reduced intestinal permeability. Honokiol repressed inflammatory response by reducing macrophage infiltration, pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 levels, and inhibiting activation of NF-κB p65 in the colitis mice. However, Sirt3 inhibitor amplified colonic oxidative stress and inflammatory response. In vitro study, Sirt3 inhibitor or siRNA Sirtuin 3 activated NF-κB p65 and enhanced TNF-α, IL-1β, and IL-6 secretion from LPS stimulated RAW264.7, while Honokiol remarkably attenuated these pro-inflammatory cytokines secretion. Finally, knockdown of Sirt3 in Caco-2 cells enhanced TNF-α induced intestinal barrier integrity injury. Sirtuin 3 negatively regulates inflammatory bowel disease progression via reducing colonic inflammation and oxidative stress. Sirtuin 3 is a promising therapeutic target in clinical application for inflammatory bowel disease therapy.

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Section: Discussionmentioning

confidence: 74%

Sirtuin 3 ameliorates inflammatory bowel disease via inhibiting intestinal inflammation and oxidative stress

Qin,

Chu,

Ding

et al. 2024

J. Clin. Biochem. Nutr.

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“…The intestinal barrier plays a critical role in safeguarding against pathogenic invasion, and its impairment can result in intestinal dysfunction, food allergies, and irritable bowel syndrome (IBS) [47,48]. Endotoxin content is a commonly employed measure of the intestinal barrier integrity [49], and the LPS group exhibited a marked increase in endotoxin content.…”

Section: Discussionmentioning

confidence: 99%

Optimum Fermentation Conditions for Bovine Lactoferricin-Lactoferrampin-Encoding LimosiLactobacillus reuteri and Regulation of Intestinal Inflammation

Xie,

Wang,

Cai

et al. 2023

Foods

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The multifunctional antibacterial peptide lactoferricin-lactoferrampin (LFCA) is derived from bovine lactoferrin. Optimization of the fermentation process should be studied since different microorganisms have their own favorable conditions and processes for growth and the production of metabolites. In this study, the culture conditions of a recombinant strain, pPG-LFCA-E/LR-CO21 (LR-LFCA), expressing LFCA was optimized, utilizing the high-density fermentation process to augment the biomass of LimosiLactobacillus reuteri and the expression of LFCA. Furthermore, an assessment of the protective effect of LR-LFCA on intestinal inflammation induced by lipopolysaccharide (LPS) was conducted to evaluate the impact of LR-LFCA on the disease resistance of piglets. The findings of this study indicate that LR-LFCA fermentation conditions optimally include 2% inoculation volume, 36.5 °C fermentation temperature, 9% dissolved oxygen concentration, 200 revolutions/minute stirring speed, pH 6, 10 mL/h glucose flow, and 50% glucose concentration. The inclusion of fermented LR-LFCA in the diet resulted in an elevation of immunoglobulin levels, significant upregulation of tight junction proteins ZO-1 and occludin, reinforcement of the intestinal barrier function, and significant amelioration of the aberrant alterations in blood physiological parameters induced by LPS. These results offer a theoretical framework for the implementation of this micro-ecological preparation in the field of piglet production to enhance intestinal well-being.

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“…Mice that are fed a HFD display a relevant reduction in the quantities of colonic ILC3s. [ 61 ] Notably, SFAs can interact with PAMPs, by mimicking LPS (i.e., interaction with toll‐like receptor (TLR) 4), thus activating the NF‐ĸB pathway. The triggered inflammatory process alters the microbiota‐GALT cross‐talk generating dysbiosis and prevalence of Th1 immune responses which contributes to chronic low‐grade inflammation.…”

Section: Differential Immunomodulatory Activities Of Fatty Acidsmentioning

confidence: 99%

High Fat Diet–Wheat Gliadin Interaction and its Implication for Obesity and Celiac Disease Onset: In Vivo Studies

Haneishi,

Treppiccione,

Maurano

et al. 2024

Molecular Nutrition Food Res

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The intestinal immune system plays a crucial role in obesity and insulin resistance. An altered intestinal immunity is associated with changes to the gut microbiota, barrier function, and tolerance to luminal antigens. Lipid metabolism and its unbalance can also contribute to acute and chronic inflammation in different conditions. In celiac disease (CD), the serum phospholipid profile in infants who developed CD is dramatically different when compared to that of infants at risk of CD not developing the disease. In a mouse model of gluten sensitivity, oral wheat gliadin challenge in connection with inhibition of the metabolism of arachidonic acid, an omega‐6 polyunsaturated fatty acid, specifically induces the enteropathy. Recent evidence suggests that gluten may play a role also for development of life‐style related diseases in populations on a high fat diet (HFD). However, the mechanisms behind these effects are not yet understood. Exploratory studies in mice feed HFD show that wheat gliadin consumption affects glucose and lipid metabolic homeostasis, alters the gut microbiota, and the immune cell profile in liver.

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Dihydromyricetin Protects Intestinal Barrier Integrity by Promoting IL-22 Expression in ILC3s through the AMPK/SIRT3/STAT3 Signaling Pathway

Cited by 10 publications

References 49 publications

Sirtuin 3 ameliorates inflammatory bowel disease via inhibiting intestinal inflammation and oxidative stress

Sirtuin 3 ameliorates inflammatory bowel disease via inhibiting intestinal inflammation and oxidative stress

Optimum Fermentation Conditions for Bovine Lactoferricin-Lactoferrampin-Encoding LimosiLactobacillus reuteri and Regulation of Intestinal Inflammation

High Fat Diet–Wheat Gliadin Interaction and its Implication for Obesity and Celiac Disease Onset: In Vivo Studies

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