ArticleCurrent medical science2021
Protective Effect of Salidroside on Mitochondrial Disturbances via Reducing Mitophagy and Preserving Mitochondrial Morphology in OGD-induced Neuronal Injury.
Article in Current medical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Assessing Dazhu Hongjingtian: Protection Against Acute Hypoxic Organ Damage and Analysis of Its Main Pharmaceutical Components.Biomedical chromatography : BMC · 2026Article
- Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury.Neural regeneration research · 2026Article
- Bioactive compounds from Chinese herbal plants for neurological health: mechanisms, pathways, and functional food applications.Frontiers in nutrition · 2025Review
- Mass Spectrometry Imaging Reveals Spatial Metabolic Alterations and Salidroside's Effects in Diabetic Encephalopathy.Metabolites · 2024Article
- Enhancing mitophagy by ligustilide through BNIP3-LC3 interaction attenuates oxidative stress-induced neuronal apoptosis in spinal cord injury.International journal of biological sciences · 2024Article
- The critical role of the endolysosomal system in cerebral ischemia.Neural regeneration research · 2023Review
- Review
- The Combination of Rhodosin and MMF Prolongs Cardiac Allograft Survival by Inhibiting DC Maturation by Promoting Mitochondrial Fusion.Oxidative medicine and cellular longevity · 2022Article
- Rhodiola Rosea Extract Counteracts Stress in an Adaptogenic Response Curve Manner via Elimination of ROS and Induction of Neurite Outgrowth.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salidroside is the active ingredient extracted from Rhodiola rosea, and has been reported to show protective effects in cerebral ischemia, but the exact mechanisms of neuronal protective effects are still unrevealed. In this study, the protective effects of salidroside (1 µmol/L) in ameliorating neuronal injuries induced by oxygen-glucose deprivation (OGD), which is a classical model of cerebral ischemia, were clarified. The results showed that after 8 h of OGD, the mouse hippocampal neuronal cell line HT22 cells showed increased cell death, accompanied with mitochondrial fragmentation and augmented mitophagy. However, the cell viability of HT22 cells showed significant restoration after salidroside treatment. Mitochondrial morphology and mitochondrial function were effectively preserved by salidroside treatment. The protective effects of salidroside were further related to the prevention of mitochondrial over-fission. The results showed that mTOR could be recruited to the mitochondria after salidroside treatment, which might be responsible for inhibiting excessive mitophagy caused by OGD. Thus, salidroside was shown to play a protective role in reducing neuronal death under OGD by safeguarding mitochondrial function, which may provide evidence for further translational studies of salidroside in ischemic diseases.
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