ArticleMolecular medicine reports2018
Simvastatin improves cerebrovascular injury caused by ischemia‑reperfusion through NF‑κB‑mediated apoptosis via MyD88/TRIF signaling.
Article in Molecular medicine reports, 2018. 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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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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Simvastatin Protects the Dopaminergic Neurons from MPTP-Mediated Injury by Inducing BDNF via PPARα Activation.Biomolecules & therapeutics · 2026Article
- The Effect of Simvastatin on the Dynamics of NF-κB-Regulated Neurodegenerative and Neuroprotective Processes in the Acute Phase of Ischemic Stroke.Molecular neurobiology · 2023Article
- Baicalein inhibits the pharmacokinetics of simvastatin in ratsPharmaceutical biology · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebrovascular injury is the most prevalent human cerebrovascular disease and frequently results in ischemic stroke. Simvastatin may be a potential therapeutic agent for the treatment of patients with cerebrovascular injury. The present study aimed to investigate the efficacy of and the potential mechanisms regulated by simvastatin in a rat model of ischemia‑reperfusion (I/R)‑induced cerebrovascular injury. Cerebrovascular injury model rats were established and were subsequently treated with simvastatin or a vehicle control following I/R injury. Cell damage, neurological functions and neuronal apoptosis were examined, as well as the nuclear factor (NF)‑κB‑mediated myeloid differentiation primary response protein 88 (MyD88)/toll‑interleukin‑1 receptor domain‑containing adapter molecule 1 (TRIF) signaling pathway following simvastatin treatment. The results of the present study demonstrated that simvastatin treatment led to a reduction in cell damage, improvement of neurological functions and decreased neuronal apoptosis compared with vehicle‑treated I/R model rats, 14 days post‑treatment. In addition, simvastatin treatment reduced cerebral water content and blood‑brain barrier disruption in cerebrovascular injury induced by I/R. The results also revealed that simvastatin treatment inhibited neuronal apoptosis via the NF‑κB‑mediated MyD88/TRIF signaling pathway. In conclusion, simvastatin treatment may reduce I/R‑induced neuronal apoptosis via inhibition of the NF‑κB‑mediated MyD88/TRIF signaling pathway.
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