ArticleJournal of experimental pharmacology2025
Andrographolide Reduces Cytokine Release and Cyclooxygenase-2 Expression by Inhibiting the JNK and NF-κB Pathways in Glioblastoma Cells Exposed to Cadmium.
Article in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Glioblastoma pathophysiology: roles of aging driven changes in STAT3 interactions with NF-κB dimer components in the modulation of the mitochondrial melatonergic pathway and night-time inflammation resolution.Exploration of targeted anti-tumor therapy · 2026Review
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Neuroinflammation is associated with brain cancer and several neurodegenerative diseases. At nontoxic concentrations, the environmental pollutant cadmium is known to increase the secretion of pro-inflammatory cytokines, including interleukin (IL)-6, IL-8, and chemokine (C-C motif) ligand 2 (CCL2) by activating the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways. Andrographolide, a diterpenoid lactone, exhibits anti-inflammatory and antioxidant activity in vitro and in vivo. Hence, in this study, we aimed to determine the effects of andrographolide on cadmium-induced inflammation and the underlying mechanisms in U-87 MG glioblastoma cells. Methods: U-87 MG cells, obtained from American Type Culture Collection (ATCC), are adherent cells derived from malignant gliomas and express the astrocyte cell marker glial fibrillary acidic protein. Cell viability was measured using the methyl thiazolyl tetrazolium (MTT) assay. Human IL-6, IL-8, and CCL2 levels were measured using enzyme-linked immunosorbent assays (ELISAs). Cyclooxygenase-2 (COX-2) and the proteins involved in the MAPK and NF-κB pathways were detected via Western blotting. Results: Treating cells with andrographolide or cadmium alone or in combination did not alter cell viability. Andrographolide decreased cadmium-induced IL-6, IL-8, and CCL2 release and downregulated cadmium-induced COX-2 expression. Andrographolide also reduced the levels of cadmium-induced phospho-Jun N-terminal kinase (JNK) and phospho-p65. Conclusion: In this study, andrographolide exerted an anti-inflammatory effect on cadmium-induced inflammation by inhibiting the JNK and NF-κB pathways. These findings have implications for the development of therapies for cadmium poisoning since the efficacy of current therapeutic approaches is limited.
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