ω-3 fatty acids attenuate mucosal inflammation in premature rat pups

Ohtsuka, Yoshikazu; Okada, Kyo; Yamakawa, Yoko; Ikuse, Tamaki; Baba, Yosuke; Inage, Eisuke; Fujii, Tohru; Izumi, Hirohisa; Oshida, Kyoichi; Nagata, Satoru; Yamashiro, Yuichiro; Shimizu, Toshiaki

doi:10.1016/j.jpedsurg.2010.07.032

Cited by 41 publications

(26 citation statements)

References 38 publications

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“…This finding is consistent with previous reports, which have shown the PUFA derivatives inhibit the LPS-induced NF-κB activation and subsequent TNF-α expression by decreased I-κBα phosphorylation and degradation [46]. In addition, recent in-vitro studies have shown that ALA has anti-inflammatory effects on HCE, which is mediated through NF-κB signal transduction [13], while n-3 PUFA inhibited NF-κB activation in an animal model of inflammation [47]. …”

Section: Discussionsupporting

confidence: 90%

Anti-inflammatory effects of resolvin-D1 on human corneal epithelial cells: in vitro study

et al. 2014

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BackgroundThis study evaluated the anti-inflammatory effects of Resolvin-D1 (RV-D1) and its mechanism of action in human corneal epithelial (HCE) cells.MethodsHCE cells were incubated with different concentrations of RV-D1 for different time periods. Oleic acid (OA) and Dexamethasone (DM) served as negative and positive controls, respectively. Cells were stimulated with polyriboinosinic:polyribocytidylic acids (poly I:C). The protein contents and mRNA expression levels of Tumor necrosis factor-α (TNF-α), Interleukin (IL)-6, IL-1β and IL-8 were evaluated with multiplex fluorescent bead immunoassay (FBI) and real time-PCR, respectively. In addition, the expression of inhibitory factor-κBα (I-κBα) was evaluated with real time-PCR.ResultsThe protein level of pro-inflammatory cytokines TNF-α, IL-6, IL-1β and IL-8 significantly increased after stimulation with Poly I:C. RV-D1 treatment at concentration of 1 μM decreased the protein level of TNF-α to 20.76 ± 9.3% (P < 0.05), IL-6 to 43.54 ± 14.16% (P < 0.001), IL-1β to 46.73 ± 15.93% (P > 0.05) and IL-8 to 51.15 ± 13.01% (P < 0.05) compared with cells stimulated with poly I:C alone. Similarly, the mRNA levels of TNF-α, IL-6, IL-1β and IL-8 were significantly reduced after treatment with RV-D1. A highly significant dose response curve was demonstrated for RV-D1 treated HCE cells for TNF-α and IL-1β.DM treatment decreased the protein content for all of the pro-inflammatory cytokines, similar results were demonstrated at the mRNA level. The anti-inflammatory effects of RV-D1 were similar to those of DM for TNF-α, IL-6 and IL-8.ConclusionsRV-D1 may serve as a potent anti-inflammatory agent in ocular surface inflammation, as evaluated in cultured HCE cells. The anti-inflammatory effects of RV-D1 were comparable to those of DM, and were mediated through nuclear factor kappa B (NF-κB) signal transduction.

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Section: Discussionsupporting

confidence: 90%

Anti-inflammatory effects of resolvin-D1 on human corneal epithelial cells: in vitro study

et al. 2014

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“…The fact indicates that PUFAs might influence CRC risk by regulating systemic inflammation status. In preneoplastic lesions of CRC, v-3 PUFAenriched diet supplementation is beneficial in a rat model of colitis via inhibition of inflammation and oxidative stress [16]. v-3 PUFAs suppress colonic polyps in a mouse model, which is possibly due to a decreased level of v-6 PUFAs in colic mucosa [17 & ].…”

Section: Role Of Polyunsaturated Fatty Acidsmentioning

confidence: 99%

Role of polyunsaturated fatty acids and lipid peroxidation on colorectal cancer risk and treatments

Cai

Dupertuis

Pichard

2012

Current Opinion in Clinical Nutrition and Metabolic Care

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Recent findings CRC is one of the most overriding threats to public health. Despite a broad range of treatments, up to 50% of patients will inevitably develop incurable metastatic disease. Peroxidation of PUFAs contributes to augmentation of oxidative stress and causes in consequence inflammation, which is one of the possible carcinogenic factors of CRC. End products of PUFAs might be used as biomarkers for CRC detection and surveillance for treatment. They also have cytotoxic effect in CRC cells. Experimental results suggest that v-3 PUFAs could increase the efficacy of radiotherapy and chemotherapy of CRC. SummaryLipid peroxidation, one factor of oxidative stress, might play a paramount role not only in carcinogenesis but also in potential therapeutic strategy on CRC. End products of lipid peroxidation, such as malondialdehyde, 4-hydroxy-2-nonenal, and isoprostanes, could be used as biomarkers for cancer detection, surveillance of treatment outcome and prognostic index for CRC patients. Furthermore, malondialdehyde and 4-hydroxy-2-nonenal have cytotoxic effect not only in normal cells but also in CRC cancer cells, which implies the potential role of PUFAs in CRC treatment.

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“…In a randomized controlled trial, enteral bovine lactoferrin supplementation decreased the incidence of NEC when combination with Lactobacillus rhamnosus GG51). In addition to the preventive strategies reviewed here, epidermal growth factor (EGF)52), heparin-binding EGF53), endothelin-1 receptor antagonist54), and ω-3 fatty acids55) may be candidates for NEC prevention, but confirmatory evidence is required.…”

Section: Preventive Strategiesmentioning

confidence: 99%

An update on necrotizing enterocolitis: pathogenesis and preventive strategies

Lee

2011

Korean J Pediatr

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Necrotizing enterocolitis (NEC) is one of the most critical morbidities in preterm infants. The incidence of NEC is 7% in very-low-birth-weight infants, and its mortality is 15 to 30%. Infants who survive NEC have various complications, such as nosocomial infection, malnutrition, growth failure, bronchopulmonary dysplasia, retinopathy of prematurity, and neurodevelopmental delays. The most important etiology in the pathogenesis of NEC is structural and immunological intestinal immaturity. In preterm infants with immature gastrointestinal tracts, development of NEC may be associated with a variety of factors, such as colonization with pathogenic bacteria, secondary ischemia, genetic polymorphisms conferring NEC susceptibility, anemia with red blood cell transfusion, and sensitization to cow milk proteins. To date, a variety of preventive strategies has been accepted or attempted in clinical practice with regard to the pathogenesis of NEC. These strategies include the use of breast feeding, various feeding strategies, probiotics, prebiotics, glutamine and arginine, and lactoferrin. There is substantial evidence for the efficacy of breast feeding and the use of probiotics in infants with birth weights above 1,000 g, and these strategies are commonly used in clinical practice. Other preventive strategies, however, require further research to establish their effect on NEC.

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ω-3 fatty acids attenuate mucosal inflammation in premature rat pups

Cited by 41 publications

References 38 publications

Anti-inflammatory effects of resolvin-D1 on human corneal epithelial cells: in vitro study

Anti-inflammatory effects of resolvin-D1 on human corneal epithelial cells: in vitro study

Role of polyunsaturated fatty acids and lipid peroxidation on colorectal cancer risk and treatments

An update on necrotizing enterocolitis: pathogenesis and preventive strategies

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