Maresin 1 attenuates the inflammatory response and mitochondrial damage in mice with cerebral ischemia/reperfusion in a SIRT1-dependent manner

Xian, Wenjing; Li, Tong; Li, Longyan; Hu, Lisha; Cao, Jian

doi:10.1016/j.brainres.2019.01.013

Cited by 50 publications

(39 citation statements)

References 36 publications

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“…Interestingly, Xian et al described a homeostatic and protective role of MaR1 on brain cerebral artery occlusion damage. MaR1 (1 ng per mice) reduced cerebral edema and the area of infarction through upregulation of Bcl-2, and a decrease in the levels of IL-6, IL-1β, and TNF-α, all related with a depletion of NF-κB nuclear translocation [33].…”

Section: Discussionmentioning

confidence: 96%

“…TNF-α acts as a pleiotropic molecule, because in the absence of Akt and NF-κB activation signaling, TNF-α mediates hepatocyte apoptosis and liver failure in mice [30]. A bulk of studies have highlighted the relation of MaR1 and the decrease of TNF-α, IL-6, and IL-1β [31][32][33][34], but they did not analyze the proliferatory potential of MaR1. Paradoxically, we found a decrease of TNF-α, but an increase in IL-6 at 3 h of perfusion, for that reason, we hypothesized that there was a prime event early in reperfusion (less than 1 h).…”

Section: Discussionmentioning

confidence: 99%

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Maresin 1, a Proresolving Lipid Mediator, Ameliorates Liver Ischemia-Reperfusion Injury and Stimulates Hepatocyte Proliferation in Sprague-Dawley Rats

Soto

Rodríguez

Fuentealba

et al. 2020

IJMS

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Maresin-1 (MaR1) is a specialized pro-resolving mediator, derived from omega-3 fatty acids, whose functions are to decrease the pro-inflammatory and oxidative mediators, and also to stimulate cell division. We investigated the hepatoprotective actions of MaR1 in a rat model of liver ischemia-reperfusion (IR) injury. MaR1 (4 ng/gr body weight) was administered prior to ischemia (1 h) and reperfusion (3 h), and controls received isovolumetric vehicle solution. To analyze liver function, transaminases levels and tissue architecture were assayed, and serum cytokines TNF-α, IL-6, and IL-10, mitotic activity index, and differential levels of NF-κB and Nrf-2 transcription factors, were analyzed. Transaminase, TNF-α levels, and cytoarchitecture were normalized with the administration of MaR1 and associated with changes in NF-κB. IL-6, mitotic activity index, and nuclear translocation of Nrf-2 increased in the MaR1-IR group, which would be associated with hepatoprotection and cell proliferation. Taken together, these results suggest that MaR1 alleviated IR liver injury, facilitated by the activation of hepatocyte cell division, increased IL-6 cytokine levels, and the nuclear localization of Nrf-2, with a decrease of NF-κB activity. All of them were related to an improvement of liver injury parameters. These results open the possibility of MaR1 as a potential therapeutic tool in IR and other hepatic pathologies.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Maresin 1, a Proresolving Lipid Mediator, Ameliorates Liver Ischemia-Reperfusion Injury and Stimulates Hepatocyte Proliferation in Sprague-Dawley Rats

Soto

Rodríguez

Fuentealba

et al. 2020

IJMS

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“…They are involved in various cellular physiological processes, such as energy metabolism, oxidative stress, and apoptosis. Their ability to resist oxidative stress has been widely studied in cerebral ischemia-reperfusion (Hou et al, 2010;Rothgiesser et al, 2010;Morris et al, 2011;She et al, 2018;Wang et al, 2018;Wu D. et al, 2018;Chang et al, 2019;Duan et al, 2019;Fusco et al, 2019;Rao et al, 2019;Xian et al, 2019;Zhao B. et al, 2019). SIRT1 activates the FOXO family, and FOXO3a has the ability to resist anti-oxidative stress and enhances ROS scavenging activity (Hou et al, 2010).…”

Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

“…SIRT1 also activates the peroxisome proliferator-activated receptor γ coactivator-1PGC1α (a transcriptional coactivator of oxidative stress) and exerts an antioxidant effect (Morris et al, 2011). By targeting SIRT1 or regulating the SIRT1 related pathway, neurons will be protected from CIRI-induced mitochondrial oxidative stress and inflammatory response (Duan et al, 2019;Fusco et al, 2019;Rao et al, 2019;Xian et al, 2019). Inflammatory cytokines can enhance the activity of SIRT2 in cells, enhance its deacetylation of NF-κB, reduce the transcriptional activity of NF-κB, and reduce the expression of inflammatory mediators, such as interleukin-6 (IL-6), matrix metalloproteinase 9 (MMP9), and cyclooxygenase-2 (COX-2), to exert antioxidant and anti-inflammatory effects (Rothgiesser et al, 2010).…”

Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

258

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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“…NPD1 regulates NFκB, and then consequently pro-inflammatory gene expression [118,139,140]. MaR1 decreases pro-inflammatory signaling cascades and influences macrophages towards an M2 repair phenotype after cerebral ischemia or spinal cord injury [141][142][143]. Figure 1.…”

Section: Introductionmentioning

confidence: 99%

n-3 Polyunsaturated Fatty Acids and Their Derivates Reduce Neuroinflammation during Aging

et al. 2020

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Aging is associated to cognitive decline, which can lead to loss of life quality, personal suffering, and ultimately neurodegenerative diseases. Neuroinflammation is one of the mechanisms explaining the loss of cognitive functions. Indeed, aging is associated to the activation of inflammatory signaling pathways, which can be targeted by specific nutrients with anti-inflammatory effects. Dietary n-3 polyunsaturated fatty acids (PUFAs) are particularly attractive as they are present in the brain, possess immunomodulatory properties, and are precursors of lipid derivates named specialized pro-resolving mediators (SPM). SPMs are crucially involved in the resolution of inflammation that is modified during aging, resulting in chronic inflammation. In this review, we first examine the effect of aging on neuroinflammation and then evaluate the potential beneficial effect of n-3 PUFA as precursors of bioactive derivates, particularly during aging, on the resolution of inflammation. Lastly, we highlight evidence supporting a role of n-3 PUFA during aging.

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Maresin 1 attenuates the inflammatory response and mitochondrial damage in mice with cerebral ischemia/reperfusion in a SIRT1-dependent manner

Cited by 50 publications

References 36 publications

Maresin 1, a Proresolving Lipid Mediator, Ameliorates Liver Ischemia-Reperfusion Injury and Stimulates Hepatocyte Proliferation in Sprague-Dawley Rats

Maresin 1, a Proresolving Lipid Mediator, Ameliorates Liver Ischemia-Reperfusion Injury and Stimulates Hepatocyte Proliferation in Sprague-Dawley Rats

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

n-3 Polyunsaturated Fatty Acids and Their Derivates Reduce Neuroinflammation during Aging

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