ArticleJournal of inflammation research2022
Alpha-Momorcharin Inhibits Proinflammatory Cytokine Expression by M1 Macrophages but Not Anti-Inflammatory Cytokine Expression by M2 Macrophages.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- LILRB3 inhibition reverses immunosuppression in glioma: a nanoparticle-based therapeutic strategy.Journal of nanobiotechnology · 2026Article
- Nanoparticle-Mediated PPAR Modulation of Macrophage Polarization in Radiation Enteritis: A Narrative Review.Drug design, development and therapy · 2026Review
- Biomimetic nanodelivery system with simultaneous blood-brain barrier-crossing and neuroprotective abilities for anti-parkinsonian therapy.Chinese medicine · 2025Article
- Functional and genomic evaluation of novel exopolysaccharide produced by marine Pediococcus pentosaceus E3 with antidiabetic, anticancer, and anti-inflammatory potentials.BMC microbiology · 2025Article
- Fractions and Compounds Obtained from Transformed Plant Cell Cultures ofPlants (Basel, Switzerland) · 2025Article
- Nutraceutical Potential of Bitter Melon (Current issues in molecular biology · 2025Review
- Inflammation preservation strategy: reconciling pain control and disc resorption in lumbar disc herniation.Frontiers in immunology · 2025Review
- Swimming upregulates APOL3 through regulating macrophage polarization to inhibit glycolysis and the development of melanoma.3 Biotech · 2024Article
- Phytochemical Composition Antioxidant and Anti-Inflammatory Activity ofAntioxidants (Basel, Switzerland) · 2024Article
- [Bioinformatics analysis and validation of the interaction between PML protein and TAB1 protein].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- MAPK Cascade Signaling Is Involved in α-MMC Induced Growth Inhibition of Multiple Myeloma MM.1S Cells via G2 Arrest and Mitochondrial-Pathway-Dependent Apoptosis In Vitro.Pharmaceuticals (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Alpha-momorcharin (α-MMC) is a natural medicine derived from bitter melon and has been found to exert immunomodulatory effects. Our previous study indicated that α-MMC can regulate cytokine release from monocytes, but it remains unknown about its regulatory effect on different types of cytokines, such as inflammatory cytokines or anti-inflammatory cytokines. Methods: LPS-induced M1-type macrophages model and IL-4-induced M2-type macrophages model were established, and the expression of proinflammatory cytokines and anti-inflammatory cytokines were assessed by ELISA after α-MMC was administered. Then, a LPS-induced acute pneumonia mouse model was established, the proinflammatory cytokines levels and inflammatory lesions in lung tissues were examined by ELISA or H&E staining. Furthermore, omics screening analysis and Western blotting verification were performed on TLR4 and JAK1-STAT6 signalling pathway-related proteins to elucidate the regulatory mechanism of α-MMC in those M1 macrophages and M2 macrophages. Results: At a noncytotoxic dose of 0.3 μg/mL, α-MMC significantly inhibited the LPS-induced expression of inflammatory cytokines, such as TNF-α, IL-1β, IL-6, IL-8, MIP-1α and MCP-1, by M1 macrophages in a time-dependent manner, but α-MMC did not inhibit the IL-4-induced synthesis of anti-inflammatory cytokines, such as IL-10, IL-1RA, EGF, VEGF, TGF-β and CCL22, by M2 macrophages. Moreover, α-MMC also inhibited inflammatory cytokine expression in an LPS-induced acute pneumonia mouse model and alleviated inflammation in lung tissues. Furthermore, omics screening and Western blotting analysis confirmed that α-MMC inhibited TAK1/p-TAK1 and subsequently blocked the downstream MAPK and NF-κB pathways, thus inhibiting the LPS-induced inflammatory cytokine expression. Conclusion: Our results reveal that α-MMC inhibits proinflammatory cytokine expression by M1 macrophages but not anti-inflammatory cytokine expression by M2 macrophages. The efficacy of α-MMC in selectively inhibiting proinflammatory cytokine expression renders it particularly suitable for the treatment of severe inflammation and autoimmune diseases characterized by cytokine storms.
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