ArticleInternational journal of molecular sciences2026
Neuroprotective Effects of Pinostrobin in a Rat Model of Kainic Acid-Induced Epilepsy.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Epilepsy is a serious neurological disorder characterized by recurrent seizures and neuronal loss. Prolonged seizure activity is associated with changes in apoptosis-related proteins, including Bcl-2-associated X protein (Bax) and caspase-3, as well as alterations in microglial and astroglial responses. This study investigated the neuroprotective effects of pinostrobin, a bioflavonoid, in a kainic acid (KA)-induced epilepsy model and examined its effects on apoptosis-related proteins. Pinostrobin (40 mg/kg) was administered orally once daily for 7 days before and 14 days after intracerebroventricular injection of KA. KA injection resulted in neuronal cell loss, increased number of ionized calcium-binding adapter molecule 1 (Iba1)-positive microglia, and reactive astrocytosis in the cornu ammonis 1 (CA1), cornu ammonis 3 (CA3), and hilar regions. These changes were accompanied by decreased levels of protein kinase B (Akt), phosphorylated-Akt (p-Akt), and the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), together with increased levels of Bax and caspase-3. Pinostrobin treatment significantly attenuated neuronal cell loss, reduced the number of Iba1-positive microglia, and increased glial fibrillary acidic protein (GFAP) immunoreactivity in the CA1, CA3, and hilar regions. Moreover, pinostrobin increased Akt, p-Akt, and Bcl-2 levels while decreasing Bax and caspase-3 levels. Collectively, these findings suggest that pinostrobin has potential neuroprotective effects in the KA-induced epilepsy model and is associated with changes in apoptosis-related proteins and glial responses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.