ArticleInflammation2019
Salidroside Reduces Inflammation and Brain Injury After Permanent Middle Cerebral Artery Occlusion in Rats by Regulating PI3K/PKB/Nrf2/NFκB Signaling Rather than Complement C3 Activity.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Salidroside Regulates DN Podocyte Injury Through the LncRNA ZEB1-AS1/miR-21-5p/PDCD4 Axis.Biochemical genetics · 2026Article
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- System-Level, Molecular and Cellular Mechanisms of Selected Plant Adaptogens-A Review.Nutrients · 2026Review
- Ferroptosis in vascular cognitive impairment: pathological mechanisms and traditional Chinese medicine interventions.Frontiers in neurology · 2026Review
- Metabolic reprogramming orchestrates microglial fate in cerebral ischemia-reperfusion injury: a spatiotemporal immunometabolic perspective.Frontiers in immunology · 2026Review
- Adaptogens in Long-Lasting Brain Fatigue: An Insight from Systems Biology and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Modulation of neuroinflammation by natural plant compounds: a promising approach for ischemic stroke.Frontiers in pharmacology · 2025Review
- Anti-Neuroinflammatory Effects of Adaptogens: A Mini-Review.Molecules (Basel, Switzerland) · 2024Review
- Phenolic Compounds ofInternational journal of molecular sciences · 2023Review
- Mechanisms of immune response and cell death in ischemic stroke and their regulation by natural compounds.Frontiers in immunology · 2023Review
- Salidroside attenuates neuronal ferroptosis by activating the Nrf2/HO1 signaling pathway in AβChinese medicine · 2022Article
- Therapeutic effects of salidroside vs pyrrolidine dithiocarbamate against severe acute pancreatitis in rat.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- The PI3K/AKT Pathway-The Potential Key Mechanisms of Traditional Chinese Medicine for Stroke.Frontiers in medicine · 2022Review
- Salidroside-pretreated mesenchymal stem cells contribute to neuroprotection in cerebral ischemic injury in vitro and in vivo.Journal of molecular histology · 2021Article
- Salidroside inhibits NLRP3 inflammasome activation and apoptosis in microglia induced by cerebral ischemia/reperfusion injury by inhibiting the TLR4/NF-κB signaling pathway.Annals of translational medicine · 2021Article
- Tianxiangdan Improves Coronary Microvascular Dysfunction in Rats by Inhibiting Microvascular Inflammation via Nrf2 Activation.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Evolution of the adaptogenic concept from traditional use to medical systems: Pharmacology of stress- and aging-related diseases.Medicinal research reviews · 2021Review
- PI3K/AKT Signal Pathway: A Target of Natural Products in the Prevention and Treatment of Alzheimer's Disease and Parkinson's Disease.Frontiers in pharmacology · 2021Review
- Neuroprotective Effect for Cerebral Ischemia by Natural Products: A Review.Frontiers in pharmacology · 2021Review
- Neuroprotective Phytochemicals in Experimental Ischemic Stroke: Mechanisms and Potential Clinical Applications.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Salidroside, an active constituent of Rhodiola rosea, is neuroprotective after transient middle cerebral artery occlusion (tMCAO). However, its effects in other experimental stroke models are less understood. Here, we investigated the effect of daily intraperitoneal injections of salidroside in rats after permanent MCAO (pMCAO). Cerebral infarct volumes at 1 day after pMCAO were significantly reduced by treatment with 100 mg/kg/day salidroside, but not by 25 or 50 mg/kg/day, and this benefit of salidroside increased significantly over at least 7 days of treatment, when it was also accompanied by decreased neurological deficit scores. These observations led us to investigate the underlying mechanism of action of salidroside. 100 mg/kg salidroside for 1 day increased NeuN, Nrf2, and its downstream mediator HO-1, while it reduced nuclear NFκB p50, IL-6, and TNFα. Brusatol, a Nrf2 inhibitor, blocked the actions of salidroside on Nrf2, NFκB p50, IL-6, and TNFα. Salidroside also increased the ratio of p-PKB/PKB at 1 day after pMCAO even in the presence of brusatol. LY294002, a PI3K inhibitor, prevented all these effects of salidroside, including those on NeuN, p-PKB/PKB, Nrf2, HO-1, and pro-inflammatory mediators. In contrast, salidroside had no significant effect on the level of cerebral complement C3 after pMCAO, or on the activity of C3 as measured by the expression of cerebral Egr1. Our findings therefore suggest that salidroside reduces neuroinflammation and neural damage by regulating the PI3K/PKB/Nrf2/NFκB signaling pathway after pMCAO, and that this neuroprotective effect does not involve modulation of complement C3 activity.
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