ArticleNeurochemical research2025
Salidroside Attenuates Epilepsy and Cognitive Dysfunction in Rats by Downregulating Complement C3-C3aR Pathway-Mediated Activation of Microglia and Astrocytes.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
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Authors and funding
3 authors.
Funding
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Abstract
Epilepsy is a chronic neurological disorder featured by abnormal neural discharges that can lead to cognitive impairment. Salidroside (Sal), a biologically active component, protects neurons against various insults. The current study aims to explore the therapeutic potential of Sal in epilepsy and elucidate the mechanisms underlying its effects. We established a rat model of status epilepticus (SE) using pentylenetetrazol-kindling. SE rats were treated with Sal. Assessment of seizure latency and epileptic stage scores were performed. Cognitive function of rats was evaluated using a novel object recognition test and a Morris water maze test. Neuronal damage and hippocampal pathology were examined, alongside microglial and astrocyte activation, complement C3-C3a receptor (C3-C3aR) pathway involvement, and inflammatory factor levels. Sal prolonged seizure latency, decreased epilepsy stage scores, and improved cognitive performance compared to untreated SE rats. Furthermore, Sal suppressed the activation of C3-C3ar, microglia, and astrocytes, while decreasing the levels of inflammatory factors, which ameliorated hippocampal damage and neuronal loss. Sal may attenuate epilepsy and cognitive dysfunction by downregulating complement C3-C3aR pathway-mediated activation of microglia and astrocytes.
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Registered trials
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