Dietary n-3 polyunsaturated fatty acids ameliorate Crohn's disease in rats by modulating the expression of PPAR-γ/NFAT

Yao, Jiayin; Lü, Yi; Mao, Zhi; Hu, Pinjin; Wu, Wei; Gao, Xiang

doi:10.3892/mmr.2017.7673

Cited by 25 publications

(19 citation statements)

References 41 publications

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“…However, the basic mechanisms have not yet been clarified. Yao et al (2017) studied the effect of n−3 PUFAs (docosahexaenoic and eicosapentaenoic acids) on TNBSinduced colitis rats, proposing a putative mechanism via the PPARg/Nuclear factor of activated T-cells (NFAT) pathway. These authors also indicated markedly decreased colonic and localized mucosal inflammation as well as gene expression of the pro-inflammatory cytokines IL-2 and IL-4.…”

Section: Pparg In CDmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptors: Experimental Targeting for the Treatment of Inflammatory Bowel Diseases

et al. 2020

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The peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that promote ligand-dependent transcription of target genes that regulate energy production, lipid metabolism, and inflammation. The PPAR superfamily comprises three subtypes, PPARa, PPARg, and PPARb/d, with differential tissue distributions. In addition to their different roles in the regulation of energy balance and carbohydrate and lipid metabolism, an emerging function of PPARs includes normal homeostasis of intestinal tissue. PPARa activation represses NF-kB signaling, which decreases the inflammatory cytokine production by different cell types, while PPARg ligands can inhibit activation of macrophages and the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-a), interleukin (IL)-6, and Il-1b. In this regard, the anti-inflammatory responses induced by PPAR activation might restore physiopathological imbalances associated with inflammatory bowel diseases (IBD). Thus, PPARs and their ligands have important therapeutic potential. This review briefly discusses the roles of PPARs in the physiopathology and therapies of the most important IBDs, ulcerative colitis (UC), and Crohn's disease (CD), as well some new experimental compounds with PPAR activity as promising drugs for IBD treatment.

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Section: Pparg In CDmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptors: Experimental Targeting for the Treatment of Inflammatory Bowel Diseases

et al. 2020

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“…Studies have shown various effects of cytokine pathways which cannot be easily integrated into a single narrative. However, elevated expression of inflammatory markers such as TNFα, IL-6, IL-1β, and IFNγ (stimulates macrophages to induce innate/adaptive immune responses), among others, and their presence in serum are frequently reported in HFD/FA-enriched rodent studies with/without induction of experimental colitis ( 14 , 50 , 51 , 75 , 79 , 105 , 106 ). Obesity-induced inflammation caused by a HFD in mice has also been shown to promote macrophage polarization toward tumor promotion via increased IL-6 ( 107 ).…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

Regulation of Intestinal Inflammation by Dietary Fats

et al. 2021

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With the epidemic of human obesity, dietary fats have increasingly become a focal point of biomedical research. Epidemiological studies indicate that high-fat diets (HFDs), especially those rich in long-chain saturated fatty acids (e.g., Western Diet, National Health Examination survey; NHANES ‘What We Eat in America’ report) have multi-organ pro-inflammatory effects. Experimental studies have confirmed some of these disease associations, and have begun to elaborate mechanisms of disease induction. However, many of the observed effects from epidemiological studies appear to be an over-simplification of the mechanistic complexity that depends on dynamic interactions between the host, the particular fatty acid, and the rather personalized genetics and variability of the gut microbiota. Of interest, experimental studies have shown that certain saturated fats (e.g., lauric and myristic fatty acid-rich coconut oil) could exert the opposite effect; that is, desirable anti-inflammatory and protective mechanisms promoting gut health by unanticipated pathways. Owing to the experimental advantages of laboratory animals for the study of mechanisms under well-controlled dietary settings, we focus this review on the current understanding of how dietary fatty acids impact intestinal biology. We center this discussion on studies from mice and rats, with validation in cell culture systems or human studies. We provide a scoping overview of the most studied diseases mechanisms associated with the induction or prevention of Inflammatory Bowel Disease in rodent models relevant to Crohn’s Disease and Ulcerative Colitis after feeding either high-fat diet (HFD) or feed containing specific fatty acid or other target dietary molecule. Finally, we provide a general outlook on areas that have been largely or scarcely studied, and assess the effects of HFDs on acute and chronic forms of intestinal inflammation.

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“…The disease activity index (DAI) of all the rats from different groups was evaluated daily according to criteria [30,31] (Table 1). Every group rats were checked the weight and euthanized at day 28.…”

Section: Assessment Of Colonic Damagementioning

confidence: 99%

Effect of Loureirin B on Crohn’s disease rat model induced by TNBS via IL-6/STAT3/NF-κB signaling pathway

Sun

Wen

et al. 2020

Chin Med

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Background: Crohn's disease (CD) is a chronic relapsing form of inflammatory bowel disease, seriously threatening human beings health. However, the pathogenesis of CD is still unclear and there is no specific effective drug for treatment of CD. Resina Donis (RD) obtained from Dracaena cochinchinensis (Lour.) S. C. Chen (Liliaceae), has been used for the treatment of CD clinically. Loureirin B (LB) is one of the most important chemical compositions and physiologically active ingredients of resina draconis. It has the molecular structure propan-1-one, 1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl)-1-(4-hydroxyphenyl)-3-(2,4,6-trimethoxyphenyl) propan-1-one. The aim of this study was to investigate the effect of LB on CD and explore the underlying mechanisms. Methods and results: In this study, the result demonstrated that LB prolonged the survival time of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rats and alleviated colonic damage in a dose dependent manner. Besides, LB remarkably ameliorated TNBS-induced inflammatory response via regulation of cytokines in the colonic tissues. Moreover, LB could reverse the established fibrosis and impede the accumulation infiltration, and improve the apoptosis induced by TNBS in a dose dependent manner. Further, LB dramatically suppressed TNBS-induced the activation of IL-6/STAT3/NF-κB signaling pathway. Conclusions: These findings suggested that LB could be beneficial regarding ameliorating TNBS-induced CD, which may represent a novel approach to treat CD and provide an alternative choice for disorders associated with CD.

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Dietary n-3 polyunsaturated fatty acids ameliorate Crohn's disease in rats by modulating the expression of PPAR-γ/NFAT

Cited by 25 publications

References 41 publications

Peroxisome Proliferator-Activated Receptors: Experimental Targeting for the Treatment of Inflammatory Bowel Diseases

Peroxisome Proliferator-Activated Receptors: Experimental Targeting for the Treatment of Inflammatory Bowel Diseases

Regulation of Intestinal Inflammation by Dietary Fats

Effect of Loureirin B on Crohn’s disease rat model induced by TNBS via IL-6/STAT3/NF-κB signaling pathway

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