Protective effects of gallic acid against cadmium-induced neuroinflammation in glioblastoma cells.
3
Issued Date
2025-01-01
Resource Type
ISSN
0732183X
eISSN
15277755
Scopus ID
2-s2.0-105039241445
Journal Title
Journal of Clinical Oncology
Volume
43
Issue
16_suppl
Start Page
e14018
End Page
e14018
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Clinical Oncology Vol.43 No.16_suppl (2025) , e14018-e14018
Suggested Citation
Phuagkhaopong S., Sukwattanasombat J., Wonganan P., Vivithanaporn P., Suknuntha K. Protective effects of gallic acid against cadmium-induced neuroinflammation in glioblastoma cells.. Journal of Clinical Oncology Vol.43 No.16_suppl (2025) , e14018-e14018. e14018. doi:10.1200/JCO.2025.43.16_suppl.e14018 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/116837
Title
Protective effects of gallic acid against cadmium-induced neuroinflammation in glioblastoma cells.
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Corresponding Author(s)
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Abstract
Background: Environmental exposure to cadmium (Cd), a toxic heavy metal, was associated with an increased incidence risk of glioblastoma multiforme (GBM), the most common, malignant primary brain tumor in adults. One possible mechanism by which Cd exerts its carcinogenic effect is related to inflammation. Our previous studies have demonstrated that Cd induces cytokine response at low concentrations (1-10 µM) and early-time points both in primary human astrocytes and human U-87 MG astrocytes. Gallic acid (GA) is a natural phenolic compound with several therapeutic effects, including anti-inflammatory, antioxidant, and anti-tumor. GA has shown a neuroprotective effect under Cd induction in Wistar rats. However, the underlying mechanism has not been extensively reported. This study aims to investigate the protective effects and potential mechanism of GA against inflammation induced by Cd exposure in human U-87 MG astrocytes. Methods: The effect of GA on Cd-induced expression and release of cytokine was investigated in human astrocytoma U-87 MG astrocytes by real-time PCR and ELISA, respectively as well as molecular mechanisms involved in the anti-inflammatory effect of this drug was investigated by Western Blotting. Results: The results showed that pretreatment of GA suppressed an increased level of interleukin (IL)-6, IL-8, chemokine (C-C motif) ligand (CCL)2, and CCL3 secretion by human U-87 MG astrocytes. In addition, pretreatment of GA inhibited Cd-activated phosphorylation of ERK1/2 MAPK and phosphorylation of signal transducer and activator of transcription 3 (STAT3). Conclusions: These findings suggest that GA may help prevent inflammation-induced GBM.