ArticleFrontiers in pharmacology2021
Gallic Acid Prevents the Oxidative and Endoplasmic Reticulum Stresses in the Hippocampus of Adult-Onset Hypothyroid Rats.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Role of gallic acid in sarcopenia in D-galactose-treated mice.Iranian journal of basic medical sciences · 2026Article
- Gallic acid showed neuroprotection against endoplasmic reticulum stress in rats.Acta cirurgica brasileira · 2025Article
- Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus.Metabolic brain disease · 2024Article
- Phikud navakot extract acts as an ER stress inhibitor to ameliorate ER stress and neuroinflammation.Heliyon · 2024Article
- The Potential Health Benefits of Gallic Acid: Therapeutic and Food Applications.Antioxidants (Basel, Switzerland) · 2024Review
- Natural Compounds as Inhibitors of Aβ Peptide and Tau Aggregation.CNS & neurological disorders drug targets · 2024Review
- Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation.Cell stress & chaperones · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Thyroid hormone is essential for hippocampal redox environment and neuronal viability in adulthood, where its deficiency causes hypothyroidism related to oxidative and endoplasmic reticulum stresses in the hippocampus, resulting in neuronal death. One option of treatment is antioxidants; however, they must be transported across the blood-brain barrier. Gallic acid is a polyphenol that meets these criteria. Thus, this study aimed to prove that the neuroprotective mechanism of GA is associated with the prevention of oxidative and endoplasmic reticulum stresses in the hippocampus of adult-onset hypothyroid rats. Male Wistar rats were divided into euthyroid (n = 20) and hypothyroid groups (n = 20). Thyroidectomy with parathyroid gland reimplementation caused hypothyroidism. Each group was subdivided into two: vehicle and 50 mg/kg/d of gallic acid. 3 weeks after thyroidectomy, six animals of each group were euthanized, and the hippocampus was dissected to evaluate oxidative and endoplasmic reticulum stress markers. The rest of the animals were euthanized after 4 weeks of treatment for histological analysis of the hippocampus. The results showed that hypothyroidism increased lipid peroxidation, reactive oxygen species, and nitrites; it also increased endoplasmic reticulum stress by activating the inositol-requiring enzyme-1α (IRE1α) pathway, the protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activated transcription factor 6α (ATF6α) pathways associated with a proapoptotic state that culminates in hippocampal neuronal damage. Meanwhile, the hypothyroid rat treated with gallic acid reduced oxidative stress and increased endoplasmic reticulum-associated degradation (ERAD) through IRE1α and ATF6. Also, the gallic acid treatment prevented the Bax/BCl2 ratio from increasing and the overexpression of p53 and caspase 12. This treatment in hypothyroid animals was associated with the neuronal protection observed in the hippocampus. In conclusion, gallic acid prevents hypothyroidism-induced hippocampal damage associated with oxidative and endoplasmic reticulum stresses.
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