ArticleJournal of molecular histology2021
Salidroside-pretreated mesenchymal stem cells contribute to neuroprotection in cerebral ischemic injury in vitro and in vivo.
Article in Journal of molecular histology, 2021. 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, 13 citations in OpenAlex.
- Bone marrow-derived mesenchymal stem cells for ischemic stroke: mechanisms, delivery strategies, clinical evidence, and translational challenges.Stem cell research & therapy · 2026Review
- Sal-hDPSCs Transplantation Alleviates Hypoxic-Ischaemic Ferroptosis in Neonatal Rats Via the FSP1-CoQInternational dental journal · 2026Article
- Mesenchymal stem cells enchanced by salidroside to inhibit ferroptosis and improve premature ovarian insufficiency via Keap1/Nrf2/GPX4 signaling.Redox report : communications in free radical research · 2025Article
- Salidroside promotes pro-angiogenesis and repair of blood brain barrier via Notch/ITGB1 signal path in CSVD Model.Journal of advanced research · 2025Article
- In vitro and In vivo Studies on Mesenchymal Stem Cells for Ischemic Stroke Therapy: A Scoping Review of The Therapeutic Effect.Stem cells and cloning : advances and applications · 2025Review
- Nootropic Herbs, Shrubs, and Trees as Potential Cognitive Enhancers.Plants (Basel, Switzerland) · 2023Review
- Apoptotic MSCs and MSC-Derived Apoptotic Bodies as New Therapeutic Tools.Current issues in molecular biology · 2022Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mesenchymal stem cells (MSCs) are considered a promising tool for treating cerebral ischemic injury. However, their poor survival after transplantation limits their therapeutic effect and applications. Salidroside has been reported to exert potent cytoprotective and neuroprotective effects. This study aimed to investigate whether salidroside could improve MSC survival under hypoxic-ischemic conditions and, subsequently, alleviate cerebral ischemic injury in a rat model. MSCs were pretreated by salidroside under hypoxic-ischemic conditions. The cell proliferation, migratory capacity, and apoptosis were evaluated by means of Cell Counting Kit-8, transwell assay, and flow cytometry. MSCs pretreated with salidroside were transplanted into the rats subsequent to middle cerebral artery occlusion. The grip strength, 2,3,5-triphenyltetrazolium chloride, and hematoxylin-eosin staining were used to analyze the therapeutic efficiency and pathological changes. The mature neuron marker NeuN and astrocyte marker GFAP in the focal area were detected by immunofluorescence. These results indicated that salidroside promoted the proliferation, migration and reduced apoptosis of MSCs under hypoxic-ischemic conditions. In vivo experiments revealed that transplantation of salidroside-pretreated MSCs strengthened the therapeutic efficiency by enhancing neurogenesis and inhibiting neuroinflammation in the hippocampal CA1 area after ischemia. Our results suggest that pretreatment with salidroside could be an effective strategy to enhance the cell survival rate and the therapeutic effect of MSCs in treating cerebral ischemic injury.
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