ArticleInflammation2018
Resolvin D1 Promotes SIRT1 Expression to Counteract the Activation of STAT3 and NF-κB in Mice with Septic-Associated Lung Injury.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Anti-Inflammatory and Antioxidant Effects of ω-3 Polyunsaturated Fatty Acids on Astrocytes and Their Implications for the Blood-Brain Barrier's Integrity and Function.International journal of molecular sciences · 2026Review
- Resolvin D1 alleviates liver inflammation and fibrosis through SIRT1-mediated NF-κB and TGF-β1/Smads pathways.Journal of inflammation (London, England) · 2026Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Article
- Article
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- Melatonin Exerts Positive Effects on Sepsis Through Various Beneficial Mechanisms.Drug design, development and therapy · 2025Review
- Review
- Resolvin D1 Inhibits IL-6-Induced Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Targeting IL-6/STAT3 Signaling.Cell biochemistry and biophysics · 2024Article
- Pharmacological effects of specialized pro-resolving mediators in sepsis-induced organ dysfunction: a narrative review.Frontiers in immunology · 2024Review
- The role and therapeutic potential of SIRTs in sepsis.Frontiers in immunology · 2024Review
- Impact of critical illness on cholesterol and fatty acids: insights into pathophysiology and therapeutic targets.Intensive care medicine experimental · 2023Review
- Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023Review
- Pre-treatment and continuous administration of simvastatin during sepsis improve metabolic parameters and prevent CNS injuries in survivor rats.Molecular and cellular biochemistry · 2022Article
- Syringaresinol Resisted Sepsis-Induced Acute Lung Injury by Suppressing Pyroptosis Via the Oestrogen Receptor-β Signalling Pathway.Inflammation · 2022Article
- Emodin alleviates sepsis-mediated lung injury via inhibition and reduction of NF-kB and HMGB1 pathways mediated by SIRT1.The Kaohsiung journal of medical sciences · 2022Article
- Resolvin D1 protects against sepsis-associated encephalopathy in mice by inhibiting neuro-inflammation induced by microglia.American journal of translational research · 2022Article
- Resolvin D1, therapeutic target in acute respiratory distress syndrome.European journal of pharmacology · 2021Review
- ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice.International journal of molecular sciences · 2021Article
- "Cell Membrane Theory of Senescence" and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resolvin D1 (RvD1) is a novel endogenous docosahexaenoic acid (DHA)-derived lipid mediators, which possesses a dual role of anti-inflammation and promotes inflammation resolution. The aim of the present study was to assess the effects of RvD1 on cecal ligation and puncture (CLP) model of sepsis and explore the underlying mechanism. Six-to-eight-week-old male C57BL/6 mice were randomly divided into following three groups: sham-operated group (SO), CLP model group (CLP), and CLP+RvD1 group (RvD1). The SO group underwent the sham operation. The RvD1 groups were administered RvD1 (10-ng/g body weight) by penile vein injection, but the CLP groups were administered the same volume of vehicle (PBS) after CLP. We assessed the survival benefit of RvD1 in CLP-induced septic mice for 7 days. After 24 h, mice were sacrificed, bronchoalveolar lavage fluids (BALF) was collected for proinflammatory cytokines assay, and albumin assay and the lung tissues were harvested for histologic analysis, myeloperoxidase (MPO) activity and the expression of Sirtuin 1 (SIRT1), signal transducers, and activators of transcription 3 (STAT3), nuclear factor-κB (NF-κB), and mitogen-activated protein kinases (MAPKs). RvD1 treatment increased the survival time in mice with sepsis induced by CLP, reducing the MPO activity and albumin level at 24 h. The levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) in BALF were significantly decreased by RvD1. RvD1 promoted SIRT1 expression and suppressed the activation of NF-κB, STAT3, ERK, and p38 in lung tissues of septic mice. These results suggest that RvD1 may improve survival and attenuate the degree of lung inflammation reaction in mice with CLP by suppressing STAT3, NF-κB, ERK, and p38 expressions through a mechanism partly dependent on SIRT1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.