ArticleMetabolic brain disease2024
Neuroprotective role of chlorogenic acid against hippocampal neuroinflammation, oxidative stress, and apoptosis following acute seizures induced by pentylenetetrazole.
Article in Metabolic brain disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Comparative Anticonvulsant Efficacy of Natural, Artificial and Cultivated Bovis Calculus in PTZ-Induced Acute Seizures.Biomedicines · 2026Article
- Advanced Green Extraction Methods for Valorising Artichoke Waste: Bioactive Composition, Stabilisation, and Implications for Nutrition and Disease Prevention.Foods (Basel, Switzerland) · 2026Review
- Chlorogenic Acid: Characteristics, Neuroprotective Effects, and Potential Mechanisms.Current neuropharmacology · 2026Review
- Metabolomics profiling and neuroprotective effects of Lagerstroemia loudonii leaf extract and its kleptose CrysmebMetabolic brain disease · 2025Article
- In Silico Exploration of Natural Antioxidants for Sepsis Drug Discovery.Molecules (Basel, Switzerland) · 2025Article
- Transforming coffee from an empirical beverage to a targeted nutritional intervention: health effects of coffee's core functional components on chronic diseases.Frontiers in nutrition · 2025Review
- Article
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Abstract
This study investigated the neuroprotective effect of chlorogenic acid (CGA) on pentylenetetrazole (PTZ)-induced acute epileptic seizures in mice. Epileptic animals received CGA (200 mg/kg) or sodium valproate (standard antiepileptic agent, 200 mg/kg) for four weeks. Results revealed that pre-administration of CGA significantly reversed the behavioral changes following pentylenetetrazole (PTZ) injection. Further, CGA pre-treatment caused significant increases in acetylcholinesterase (AChE) activity and brain-derived neurotrophic factor (BDNF) levels, along with marked increases in dopamine, norepinephrine, and serotonin levels. Additionally, the increased antioxidant enzymes activities, along with higher glutathione (GSH) contents and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) gene expression, were indicative of a notable improvement in the cellular antioxidant defense in mice treated with CGA. These results were associated with lowered malondialdehyde (MDA) and nitric oxide (NO) levels. Moreover, epileptic mice that received CGA showed significant declines in the content of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and nuclear factor kappa-B (NF-κB), besides downregulating inducible nitric oxide synthase (iNOS) expression. Remarkably, CGA counteracted hippocampal apoptosis by lessening the levels of pro-apoptotic biomarkers [Bcl-2-associated X protein (Bax) and caspase-3] and increasing the anti-apoptogenic marker level of B-cell lymphoma 2 (Bcl-2). The hippocampal histopathological findings corroborated the abovementioned changes. In sum, these findings suggest that CGA could mediate the neuroprotective effect against PTZ-induced epilepsy via modulation of neurotransmitters, oxidative damage, neuroinflammation, and apoptosis. CGA, therefore, could be considered a valuable antiepileptic therapeutic supplement.
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