ArticleInflammation2014
Magnolol inhibits tumor necrosis factor-α-induced ICAM-1 expression via suppressing NF-κB and MAPK signaling pathways in human lung epithelial cells.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- The Cardioprotective Effect ofInternational journal of molecular sciences · 2025Review
- Jing Guan Fang, an herbal formula, as an immunomodulator: opposing effects on basal and lipopolysaccharide-induced inflammation of macrophage via JAK/STAT3 and MAPK pathways.Frontiers in pharmacology · 2025Article
- Pharmacodynamics and Cellular Uptake of Peimine and Peiminine in Inflammatory Model Non-Small-Cell Lung Cancer Epithelial Cells (A549).Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Systematic Review: Guideline-Based Approach for the Management of Asthma and Subtypes via Chinese Medicine.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- The Protective Effects of Maresin 1 in the OVA-Induced Asthma Mouse Model.Mediators of inflammation · 2021Article
- Magnolol additive improves growth performance of Linwu ducklings by modulating antioxidative status.PloS one · 2021Article
- Article
- Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update.Frontiers in pharmacology · 2021Review
- Article
- Insights on the Multifunctional Activities of Magnolol.BioMed research international · 2019Review
- The Protective Effect of Magnolol in Osteoarthritis:Frontiers in pharmacology · 2019Article
- 9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells.Scientific reports · 2018Article
- PMParticle and fibre toxicology · 2018Article
- Magnolol additive as a replacer of antibiotic enhances the growth performance ofAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2017Article
- Theophylline action on primary human bronchial epithelial cells under proinflammatory stimuli and steroidal drugs: a therapeutic rationale approach.Drug design, development and therapy · 2017Article
- Methylation and Esterification of Magnolol for Ameliorating Cutaneous Targeting and Therapeutic Index by Topical Application.Pharmaceutical research · 2016Article
- Magnolol pretreatment attenuates heat stress-induced IEC-6 cell injury.Journal of Zhejiang University. Science. B · 2016Article
- Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways.Acta pharmacologica Sinica · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Magnolol is a traditional Chinese medicine from the root and bark of Magnolia officinalis. It has long been used to treat anxiety, cough, headache and allergies, as well as a variety of inflammations. Lung inflammation is a key event in the pathogenesis of asthma and chronic obstructive pulmonary disease. The present study sought to examine the effects of magnolol on tumor necrosis factor (TNF)-α-induced upregulation of intercellular adhesion molecule-1 (ICAM-1), activation of the nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathway in cultured human pulmonary epithelial cells, and adhesion of human macrophage-like U937 cells to A549 cells. A549 cells were incubated with magnolol at 25 and 50 μmol/l. Then, 20 ng/ml TNF-α was used to activate the cells. Magnolol inhibited the growth of human pulmonary epithelial A549 cells in a dose- and time-dependent manner. Magnolol suppressed the adhesion of U937 cells to TNF-α-induced A549 cells. In cultured human pulmonary epithelial A549 cells, magnolol decreased TNF-α-induced upregulation of ICAM-1. Magnolol repressed TNF-α-induced activation of NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways in A549 cells by inhibiting phosphorylation of NF-κB, p38, extracellular signal-regulated kinase (ERK) 1/2, and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK). These findings support the hypothesis that magnolol inhibits the inflammatory process in lung epithelial A549 cells by suppressing the ICAM-1 and NF-κB and MAPK signaling pathways. Taken together, these results indicate that magnolol offers significant potential as a therapeutic treatment for inflammatory diseases of the lungs including asthma, sepsis, and chronic obstructive pulmonary disease.
Indexed as
Identifiers
What OpenQuestion holds
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.