ArticleBMC complementary medicine and therapies2024
The effect of salidroside in promoting endogenous neural regeneration after cerebral ischemia/reperfusion involves notch signaling pathway and neurotrophic factors.
Article in BMC complementary medicine and therapies, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Natural Products and Neuroregeneration: Rethinking Discovery Beyond Bioavailability Through Pseudo-Natural Product Design.Biomedicines · 2026Review
- Review
- ErbB signaling in brain injury regeneration: Pathway interactions and therapeutic potential.Neural regeneration research · 2026Article
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- Adeno-associated virus-mediated inhibition of ROCK2 promotes synaptogenesis and neurogenesis in rats after ischemic stroke.Neural regeneration research · 2026Article
- Salidroside Alleviates Fluoride-Induced Pyroptosis and Developmental Neurotoxicity Through P2X7R/NF-κB/NLRP3 Pathway.Biological trace element research · 2026Article
- Identification of Dopamine D2 Receptor as a Direct Target of Salidroside and Tyrosol by Integrated Transcriptomic and Biophysical Approaches.Pharmaceuticals (Basel, Switzerland) · 2026Article
- System-Level, Molecular and Cellular Mechanisms of Selected Plant Adaptogens-A Review.Nutrients · 2026Review
- Protective Effect of Salidroside Against Multiple Organs Ischemia-Reperfusion Injury: New Insights From Common and Specific Pharmacological Mechanisms.Drug design, development and therapy · 2026Review
- Neuroprotective effects of salidroside against cerebral ischemia-reperfusion injury involve downregulation of total NAMPT and suppression of microglial inflammation.Frontiers in pharmacology · 2026Article
- Salidroside Alleviates Renal Ischemia-reperfusion Injury by Inhibiting Macrophage Pyroptosis Through HIF Signaling.Inflammation · 2025Article
- A comprehensive review on adaptive plasticity and recovery mechanisms post-acquired brain injury.Neuroprotection (Chichester, England) · 2025Review
- bFGF-Mediated Inhibition of Astrocytes' Optogenetic Activation Impairs Neuronal Repair in Female Rats After Stroke.International journal of molecular sciences · 2025Article
- Adaptogens in Long-Lasting Brain Fatigue: An Insight from Systems Biology and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Bioactive compounds from Chinese herbal plants for neurological health: mechanisms, pathways, and functional food applications.Frontiers in nutrition · 2025Review
- Article
- Targeting astrocytes polarization after spinal cord injury: a promising direction.Frontiers in cellular neuroscience · 2024Review
- Expression of BDNF in the Cortex and Hippocampus of Mice With Middle Cerebral Artery Occlusion.In vivo (Athens, Greece)Article
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Abstract
backgroundSalidroside is the major bioactive and pharmacological active substance in Rhodiola rosea L. It has been reported to have neuroprotective effects on cerebral ischemia/reperfusion (I/R). However, whether salidroside can enhance neural regeneration after cerebral I/R is still unknown. This study investigated the effects of salidroside on the endogenous neural regeneration after cerebral I/R and the related mechanism.
methodsFocal cerebral I/R was induced in rats by transient middle cerebral artery occlusion/reperfusion (MCAO/R). The rats were intraperitoneally treated salidroside once daily for 7 consecutive days. Neurobehavioral assessments were performed at 3 days and 7 days after the injury. TTC staining was performed to assess cerebral infarct volume. To evaluate the survival of neurons, immunohistochemical staining of Neuronal Nuclei (NeuN) in the ischemic hemisphere were conducted. Also, immunofluorescence double or triple staining of the biomarkers of proliferating neural progenitor cells in Subventricular Zone (SVZ) and striatum of the ischemia hemisphere were performed to investigate the neurogenesis. Furthermore, reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of neurotrophic factors (NTFs) brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). Expression of Notch1 and its target molecular Hes1 were also analyzed by western-blotting and RT-PCR.
resultsSalidroside treatment ameliorated I/R induced neurobehavioral impairment, and reduced infarct volume. Salidroside also restored NeuN positive cells loss after I/R injury. Cerebral I/R injury significantly increased the expression of 5-Bromo-2'-Deoxyuridine (BrdU) and doublecotin (DCX), elevated the number of BrdU/Nestin/DCX triple-labeled cells in SVZ, and BrdU/Nestin/glial fibrillary acidic protein (GFAP) triple-labeled cells in striatum. Salidroside treatment further promoted the proliferation of BrdU/DCX labeled neuroblasts and BrdU/Nestin/GFAP labeled reactive astrocytes. Furthermore, salidroside elevated the mRNA expression and protein concentration of BDNF and NGF in ischemia periphery area, as well. Mechanistically, salidroside elevated Notch1/Hes1 mRNA expression in SVZ. The protein levels of them were also increased after salidroside administration.
conclusionsSalidroside enhances the endogenous neural regeneration after cerebral I/R. The mechanism of the effect may involve the regulation of BDNF/NGF and Notch signaling pathway.
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