ArticleBiochemical genetics2025
Gastrodin Attenuates Neuroinflammation and Injury in Young Rats with LiCl/Pilocarpine-Induced Status Epilepticus.
Article in Biochemical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Protective effects of gastrodin against bisphenol A-induced dopaminergic dysregulation and cognitive impairment in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulatory Effects of Bioactive Phytoconstituents on the Amplitude and Gating Properties of Membrane Ion Channels.Molecules (Basel, Switzerland) · 2026Review
- Gastrodin alleviates neuronal damage in epileptic cell models by targeting P2RY12 to inhibit microglial hyperactivation.PloS one · 2026Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Status epilepticus is a severe neurological emergency that often leads to long-term neuronal damage and functional impairment. Gastrodin is a compound widely used in traditional Chinese medicine with potential neuroprotective effects. This study aims to investigate the effects of GAS on neuroinflammation and injury caused by LiCl/pilocarpine-induced SE in young rats. SE in rats was induced using the LiCl/pilocarpine model. Morris water maze and Y-maze experiments were used for the behavioral test of rats. Enzyme-linked immunosorbent assay was utilized to quantify the levels of interleukin (IL)-1β, IL-6, and IL-8 levels, and biochemical kits assessed the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase (GSH-px) in hippocampus tissues. Additionally, Western blot analysis was performed to evaluate the protein expression levels of p-p65, p65, p-IκBα and IκBα, which are key factors of the nuclear factor kappa B (NF-κB) signaling pathway. Compared to the control group, the SE group rats exhibited reduced learning and memory abilities. Markedly elevated levels of inflammatory factors (IL-1β, IL-6, and IL-8). The expression levels of p-p65 and p-IκBα were significantly upregulated, while IκBα levels were notably decreased. Following GAS treatment, the latency of seizure onset was significantly shortened, the incidence of SE was significantly reduced and the severity of nerve injury was alleviated. Additionally, both the inflammation levels and the oxidative stress were significantly decreased, primarily through inhibition NF-κB signaling pathway. These findings suggest that GAS may be a potential therapeutic agent for treating SE.
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