Resolvin D1 protects against hepatic ischemia/reperfusion injury in rats

Zhang, Tao; Shu, Haihua; Chang, Lu; Ye, Fang; Xu, Kan; Huang, Wenqi

doi:10.1016/j.intimp.2015.06.017

Cited by 30 publications

(16 citation statements)

References 31 publications

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“…The reduction in tumor necrosis factor-a and IL-6 (pyrogenic cytokines) is an action also shared with RvD1, RvD2, and RvD3. 26,27 PCTR1 shares substrate intermediates with PD1 and D-series resolvins. 7,13 Distinctly, PCTR1 at 1 nmol/L did not affect IL-10 levels (data not shown), a known function of PD1 and RvD1.…”

Section: Discussionmentioning

confidence: 99%

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

Ramon

Dalli

Sanger

et al. 2016

The American Journal of Pathology

115

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Inflammation and its natural resolution are host-protective responses triggered by infection or injury. The resolution phase of inflammation is regulated by enzymatically produced specialized pro-resolving mediators. We recently identified a new class of peptide-conjugated specialized pro-resolving mediators that carry potent tissue regenerative actions that belong to the protectin family and are coined protectin conjugates in tissue regeneration (PCTR). Herein, with the use of microbial-induced peritonitis in mice and liquid chromatography-tandem mass spectrometryebased lipid mediator metabololipidomics, we found that PCTR1 is temporally regulated during self-resolving infection. When administered at peak of inflammation, PCTR1 enhanced macrophage recruitment and phagocytosis of Escherichia coli, decreased polymorphonuclear leukocyte infiltration, and counter-regulated inflammation-initiating lipid mediators, including prostaglandins. In addition, biologically produced PCTR1 promoted human monocyte and macrophage migration in a dose-dependent manner (0.001 to 10.0 nmol/L). We prepared PCTR1 via organic synthesis and confirmed that synthetic PCTR1 increased macrophage and monocyte migration, enhanced macrophage efferocytosis, and accelerated tissue regeneration in planaria. With human macrophage subsets, PCTR1 levels were significantly higher in M2 macrophages than in M1 phenotype, along with members of the resolvin conjugates in tissue regeneration and maresin conjugate families. In contrast, M1 macrophages gave higher levels of cysteinyl leukotrienes. Together, these results demonstrate that PCTR1 is a potent monocyte/macrophage agonist, regulating key anti-inflammatory and pro-resolving processes during bacterial infection. (Am J Pathol 2016, 186: 962e973; http://dx

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Section: Discussionmentioning

confidence: 99%

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

Ramon

Dalli

Sanger

et al. 2016

The American Journal of Pathology

115

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“…Due to its lack of adverse side effects, AT-RvD1 offers an attractive alternative option to the use of corticosteroids. RvD1 has shown to be useful in treating a variety of conditions such as experimental colitis, alveolar epithelial cell injury, smoke-induced lung inflammation, colon cancer, rheumatoid arthritis, chronic obstructive pulmonary disease, ischemic injuries and uveitis [27–34]. Moreover, our previous in vitro studies indicate that RvD1 and AT-RvD1 block inflammatory signals in the rat parotid Par-C10 cell line and in freshly isolated submandibular gland cells [13,14], suggesting a potential therapeutic benefit for SS in vivo .…”

Section: Discussionmentioning

confidence: 99%

Aspirin-Triggered Resolvin D1 Versus Dexamethasone in the Treatment of Sjögren's Syndrome-Like NOD/ShiLtJ Mice - A Pilot Study

et al. 2015

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Resolvin D1 (RvD1) and its aspirin-triggered epimeric form (AT-RvD1) are endogenous lipid mediators (derived from docosahexaenoic acid, DHA) that control the duration and magnitude of inflammation in models of complex diseases. Our previous studies demonstrated that RvD1-mediated signaling pathways are expressed and active in salivary glands from rodents and humans. Furthermore, treatment of salivary cells with RvD1 blocked TNF-α-mediated inflammatory signals and improved epithelial integrity. The purpose of this pilot study was to determine the feasibility of treatment with AT-RvD1 versus dexamethasone (DEX) on inflammation (i.e., lymphocytic infiltration, cytokine expression and apoptosis) observed in submandibular glands (SMG) from the NOD/ShiLtJ Sjögren’s syndrome (SS) mouse model before experimenting with a larger population. NOD/ShiLtJ mice were treated intravenously with NaCl (0.9%, negative control), AT-RvD1 (0.01–0.1 mg/kg) or DEX (4.125–8.25 mg/kg) twice a week for 14 weeks beginning at 4 weeks of age. At 18 weeks of age, SMG were collected for pathological analysis and detection of SS-associated inflammatory genes. The AT-RvD1 treatment alone did not affect lymphocytic infiltration seen in NOD/ShiLtJ mice while DEX partially prevented lymphocytic infiltration. Interestingly, both AT-RvD1 and DEX caused downregulation of SS-associated inflammatory genes and reduction of apoptosis. Results from this pilot study suggest that a systemic treatment with AT-RvD1 and DEX alone attenuated inflammatory responses observed in the NOD/ShiLtJ mice; therefore, they may be considered as potential therapeutic tools in treating SS patients when used alone or in combination.

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“…A recent study has evaluated the effect of intravenous injection of RvD1 (5 µg/kg) in an experimental model of hepatic ischemia/reperfusion. The authors of the study found that pretreatment with RvD1 is protective by decreasing cytokine production (IL‐6, TNF‐α, and myeloperoxidase), by inhibiting apoptosis through an increased Akt phosphorylation . In an experimental model of vascular injury, treatment with RVD2 or maresin 1 was associated with a reduced cell migration, a decreased recruitment of immune cell and a decreased NF‐κB activation .…”

Section: Eicosanoidsmentioning

confidence: 98%

Polyunsaturated fatty acids and inflammation

2015

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Inflammation is a protective process for life that aims to restore body homeostasis by targeting the injury and by inducing repair mechanisms. This process can also become excessive and lead to chronic inflammation and organ fibrosis. Polyunsaturated fatty acids play a key role in inflammatory processes and their resolution. Indeed, numerous lipid mediators derived from n-3 or n-6 PUFA such as eicosanoids, endocannabinoids, or proresolving lipids are able to target transcription factors to modulate gene expression. One other important action mechanism is by modification of cell membrane composition. The purpose of the present review is to describe the potential mechanisms by which PUFA influence inflammatory processes. To illustrate this purpose, we focused on the interactions between PUFA and intestinal inflammation as an integrative example. V C 2015 IUBMB Life, 67(9):659-667, 2015

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Resolvin D1 protects against hepatic ischemia/reperfusion injury in rats

Cited by 30 publications

References 31 publications

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

The Protectin PCTR1 Is Produced by Human M2 Macrophages and Enhances Resolution of Infectious Inflammation

Aspirin-Triggered Resolvin D1 Versus Dexamethasone in the Treatment of Sjögren's Syndrome-Like NOD/ShiLtJ Mice - A Pilot Study

Polyunsaturated fatty acids and inflammation

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