ArticleMolecular and cellular biochemistry2026
Gallic acid partially attenuates thiomersal-associated oxidative, apoptotic, and CREB/BDNF-related alterations in rat hippocampal and prefrontal cortex tissues and systemic inflammatory responses.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Thiomersal (THIM), an organomercury preservative, has been associated with oxidative stress-related neurotoxicity. This study investigated the effects of gallic acid (GA) on THIM-associated oxidative, apoptotic, and CREB/BDNF-related molecular alterations in brain tissue and systemic inflammatory responses in rats. Twenty-eight male Wistar albino rats were assigned to Control, THIM, GA, and THIM+GA groups (n = 7/group). THIM (25 µg/kg, intraperitoneally) was administered at 10-day intervals, whereas GA (50 mg/kg/day, oral gavage) was given for 20 consecutive days. MDA, SOD, CAT, and GSH were measured in combined hippocampal and prefrontal cortex homogenates; serum MDA, IL-1β, IL-6, and TNF-α were also assessed. Bax, Bcl-2, Casp-3, CREB, and BDNF mRNA expression was analyzed by RT-qPCR. THIM increased tissue MDA (0.44 ± 0.06 vs. 1.06 ± 0.15 nmol/mg protein, p < 0.0001) and serum TNF-α (93.9 ± 9.6 vs. 171.3 ± 8.8 ng/L, p < 0.0001) and reduced BDNF mRNA expression (1.01 ± 0.15 vs. 0.41 ± 0.17, p = 0.0001). In THIM-exposed animals, GA reduced tissue MDA and serum TNF-α and increased BDNF expression (all p < 0.05). Significant THIM × GA interactions were identified for tissue CAT, GSH, MDA, Bax/Bcl-2 ratio, BDNF, and serum MDA, IL-1β, IL-6, and TNF-α. Simple-effects analyses indicated that GA effects were mainly evident during THIM exposure. These findings suggest that GA partially attenuates THIM-associated oxidative and apoptosis-related molecular alterations, systemic inflammatory responses, and BDNF-related transcriptional changes.
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