ArticleJournal of inflammation (London, England)2020
Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of granulocytes.
Article in Journal of inflammation (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Effect of emodin on acute lung injury: a meta-analysis of preclinical trials.BMC pulmonary medicine · 2024Pooled it
- Systematically investigate the mechanism underlying the therapeutic effect of emodin in treatment of prostate cancer.Discover oncology · 2025Article
- Emodin promotes the recovery of rheumatoid arthritis by regulating the crosstalk between macrophage subsets and synovial fibroblast subsets.Animal models and experimental medicine · 2025Article
- Sodium Houttuyniae attenuates ferroptosis by regulating TRAF6-c-Myc signaling pathways in lipopolysaccharide-induced acute lung injury (ALI).BMC pharmacology & toxicology · 2024Article
- Anti-Inflammatory Activity of Peptides fromFoods (Basel, Switzerland) · 2024Article
- Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis.Neural regeneration research · 2023Article
- Article
- Traditional Chinese medicine for treatment of sepsis and related multi-organ injury.Frontiers in pharmacology · 2023Review
- Mechanism of Emodin in the Treatment of Rheumatoid Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Friend or Foe? The Roles of Antioxidants in Acute Lung Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial Protection and Anti-inflammatory Effects Induced by Emodin in the Human Neuroblastoma SH-SY5Y Cells Exposed to Hydrogen Peroxide: Involvement of the AMPK/Nrf2 Signaling Pathway.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of granulocytes (mainly neutrophils) that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the granulocytes function in a rat model of lipopolysaccharide (LPS)-induced ALI.
resultsTreatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with granulocyte deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced granulocytes via the up-regulation of the ability of granulocytes to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated granulocytes, alleviating the damage of granulocytes to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of granulocytes.
conclusionOur results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of granulocytes. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.
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