ArticleArchives of medical science : AMS2021
Salidroside regulates imbalance of Th17/Treg and promotes ischemic tolerance by targeting STAT-3 in cerebral ischemia-reperfusion injury.
Article in Archives of medical science : AMS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Overexpression of PGC-1α reduces inflammation and protects against focal cerebral ischaemia/reperfusion injury.Archives of medical science : AMS · 2026Article
- Protective Effect of Salidroside Against Multiple Organs Ischemia-Reperfusion Injury: New Insights From Common and Specific Pharmacological Mechanisms.Drug design, development and therapy · 2026Review
- Salidroside and inflammation-linked disorders: integrative insights into the pharmacological effects and mechanistic targets.Inflammopharmacology · 2025Review
- Salidroside Attenuates Cerebral Ischemia-Reperfusion Injury via ERβ/BNIP3-Mediated Mitochondrial Autophagy Activation in a Rat Model.Neurochemical research · 2025Article
- The Role of IL-17A in Mediating Inflammatory Responses and Progression of Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Evaluating the effect of the antiPCSK9 vaccine on systemic inflammation and oxidative stress in an experimental mouse model.Cardiology journal · 2025Article
- The critical role of Th17 cells and IL-17A in autoimmune and inflammation-associated neurological diseases: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Cellular therapy for traumatic brain injury in adults: a meta-analysis of controlled clinical trials.Archives of medical science : AMS · 2025Review
- Resolving candidate genes of duck ovarian tissue transplantation via RNA-Seq and expression network analyses.Poultry science · 2024Article
- Th17 Cells and IL-17A in Ischemic Stroke.Molecular neurobiology · 2024Review
- Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2023Article
- Article
- CD39 molecule: a negative regulator expressed on T cells in patients with lung adenocarcinoma.Archives of medical science : AMS · 2023Article
- Pharmacological functions of salidroside in renal diseases: facts and perspectives.Frontiers in pharmacology · 2023Review
- Salidroside attenuates HALI via IL-17A-mediated ferroptosis of alveolar epithelial cells by regulating Act1-TRAF6-p38 MAPK pathway.Cell communication and signaling : CCS · 2022Article
- Therapeutic potential and molecular mechanisms of salidroside in ischemic diseases.Frontiers in pharmacology · 2022Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe balance between Th17 and Treg cells controls the immune response and is an important regulator of helper T cells acting on autoimmune diseases. Focal cerebral ischemia-reperfusion injury can induce imbalance of Th17/Treg cells in the brain and the peripheral immune system of rats. The aim of this study was to investigate the effect of salidroside (Sal) on the ratio of Th17 and Treg cells in an adult rat model of middle cerebral artery occlusion (MCAO). MATERIAL AND
methodsForty rats were divided into 4 groups: normal group, sham group, surgery group, and Sal group. After treatment, the neurological deficits in rats were evaluated. Peripheral blood mononuclear cells were isolated and the count of Th17 and Treg cells was detected by flow cytometry. The infarct size and expression of RORγt and Foxp3 were detected in rat brain tissue. Rat spleen cells were isolated, CD4
resultsThe results show that MCAO can induce an imbalance of Th17 and Treg cells in peripheral blood of rats. Sal treatment can significantly reduce the neurological deficit and infarct size of MCAO rats, reverse the oxidative stress of rat brain tissue, and inhibit the apoptosis of brain cells in MCAO rats. In the brain tissue of MCAO rats, Sal could significantly inhibit the expression of IL-6, TNF-α, MCP-1, STAT-3 and NF-κ-B2. Down-regulation of STAT-3 significantly reversed the therapeutic effects of Sal treatment.
conclusionsOur results indicate that Sal can increase the tolerance of rat brain tissue to ischemia, inhibit cell apoptosis and reduce oxidative stress by targeting STAT-3.
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