ArticleBMC veterinary research2021
Metformin activated AMPK signaling contributes to the alleviation of LPS-induced inflammatory responses in bovine mammary epithelial cells.
Article in BMC veterinary research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Metformin as an Innate Immune Modulator: Metabolic and Epigenetic Reprogramming of Innate Immune Cells and Therapeutic Implications.Current issues in molecular biology · 2026Review
- Repurposing metformin as a dual-function agent to combat E. coli-induced mastitis: Mechanistic insights into biofilm dispersion and AMPK/SIRT1-mediated NF-κB inhibition.PLoS pathogens · 2026Article
- New Frontiers for Old Medications: Repurposing Approved Drugs Against Gram-Negative Bacterial Infections.Microorganisms · 2025Review
- The Possible Role of Metformin and Fibroblast Growth Factor-21 in Multiple Sclerosis Neuropathology: Birds of a Feather Flock Together.The European journal of neuroscience · 2025Review
- NLRP3 inflammasomes pathway: a key target for Metformin.Inflammopharmacology · 2025Review
- H3K14: A histone site closely related to diseases.Journal of Cancer · 2025Review
- Analysis of the fecal microbiome and metabolome in dairy cows with different body condition scores.PloS one · 2025Article
- AMP-activated protein kinase mediates (-)-epigallocatechin-3-gallate (EGCG) to promote lipid synthesis in mastitis cows.Animal biotechnology · 2024Article
- Bioactive Compounds and Probiotics Mitigate Mastitis by Targeting NF-κB Signaling Pathway.Biomolecules · 2024Review
- Article
- Metformin: The Winding Path from Understanding Its Molecular Mechanisms to Proving Therapeutic Benefits in Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2023Review
- PasteurizedNutrients · 2022Article
- Exploring the Pharmacological Potential of Metformin for Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- The protective role of caffeic acid on bovine mammary epithelial cells and the inhibition of growth and biofilm formation of Gram-negative bacteria isolated from clinical mastitis milk.Frontiers in immunology · 2022Article
- Lycium barbarum polysaccharides alleviate LPS-induced inflammatory responses through PPARγ/MAPK/NF-κB pathway in bovine mammary epithelial cells.Journal of animal science · 2022Article
- Metformin Therapy Attenuates Pro-inflammatory Microglia by Inhibiting NF-κB in Cuprizone Demyelinating Mouse Model of Multiple Sclerosis.Neurotoxicity research · 2021Article
- Growth Factors, Reactive Oxygen Species, and Metformin-Promoters of the Wound Healing Process in Burns?International journal of molecular sciences · 2021Review
- Metformin acts to suppress β-hydroxybutyric acid-mediated inflammatory responses through activation of AMPK signaling in bovine hepatocytes.Journal of animal science · 2021Article
- Inhibition of Lipopolysaccharide-Induced Inflammatory and Oxidative Responses byInternational journal of medical sciences · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLipopolysaccharides (LPS) derived from gram-negative bacterial are often regarded as primary inducer of bovine mammary inflammation. This study evaluated the biological response of metformin activated AMPK signaling on LPS-induced inflammatory responses and metabolic changes in primary bovine mammary epithelial cells (pbMEC). The pbMEC were exposed to either 3 mmol/L Metf. for 12 h as Metf. group (Metf.) or 2 μg/mL LPS for 6 h as LPS group (LPS). Cells pretreated with 3 mmol/L metformin for 12 h followed by washing and 2 μg/mL LPS exposure for 6 h were served as ML group (ML). PBS was added to cells as the control group (Con.).
resultsPre-incubation with Metf. inhibited LPS-induced expression of pro-inflammatory genes (TNF, IL1B, IL6, CXCL8, MYD88 and TLR4) and proteins (IL-1β, TNF-α, NLRP3, Caspase1, ASC) and was accompanied by increased activation of AMPK signaling. Compared with the LPS group, phosphorylation of p65 and IκBα in the ML group were decreased and accumulation of NF-κB in the nucleus was significantly reduced by pretreatment with metformin. Metformin protects the cells from the increase of LPS-induced binding activity of NF-κB on both TNFA and IL1B promoters. Compared with the LPS group, genes (G6PC, PCK2) and proteins (SREBP1, SCD1) related to lipogenesis and carbohydrate metabolism were downregulated while catabolic ones (PPARA, ACSL1, Glut1, HK1) were upregulated in the ML group. Furthermore, increased acetylation of H3K14 by LPS challenge was reversed by pretreatment with metformin.
conclusionAltogether, our results indicated that pretreatment with metformin dampens LPS-induced inflammatory responses mediated in part by AMPK/NF-κB/NLRP3 signaling and modification of histone H3K14 deacetylation and metabolic changes.
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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 Socratic graph.