ArticleInternational journal of molecular sciences2014
Inhibitory effects of palmultang on inflammatory mediator production related to suppression of NF-κB and MAPK pathways and induction of HO-1 expression in macrophages.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Modulation of Bovine Endometrial Cell Receptors and Signaling Pathways as a Nanotherapeutic Exploration against Dairy Cow Postpartum Endometritis.Animals : an open access journal from MDPI · 2021Review
- Article
- Andrographolide Derivative AL-1 Ameliorates Dextran Sodium Sulfate-Induced Murine Colitis by Inhibiting NF-Oxidative medicine and cellular longevity · 2019Article
- Beneficial Effects of Gagam-Palmultang on Scopolamine-Induced Memory Deficits in Mice.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Hesperetin Suppresses Inflammatory Responses in Lipopolysaccharide-Induced RAW 264.7 Cells via the Inhibition of NF-κB and Activation of Nrf2/HO-1 Pathways.Inflammation · 2016Article
- Molecular science for drug development and biomedicine.International journal of molecular sciences · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Palmultang (PM) is an herbal decoction that has been used to treat anorexia, anemia, general prostration, and weakness due to chronic illness since medieval times in Korea, China, and Japan. The present study focused on the inhibitory effects of PM on the production of inflammatory factors and on the activation of mechanisms in murine macrophages. PM suppressed the expression of nitric oxide (NO), inflammatory cytokines and inflammatory proteins by inhibiting nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) signaling pathways and by inducing heme oxygenase (HO)-1 expression. Collectively, our results explain the anti-inflammatory effect and inhibitory mechanism of PM in macrophages stimulated with lipopolysaccharide (LPS).
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