ArticleNeuropsychiatric disease and treatment2020
Tanshinone IIA Promotes M2 Microglia by ERβ/IL-10 Pathway and Attenuates Neuronal Loss in Mouse TBI Model.
Article in Neuropsychiatric disease and treatment, 2020. 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, 20 citations in OpenAlex.
- Enhanced neuroprotection effects of transcranial direct current stimulation combined with 6-Gingerol in copper-overloaded traumatic brain injury via mGluR1.Biology direct · 2026Article
- Synergistic effects of tanshinone IIA and mesenchymal stem cells on neuroprotection, cardiovascular repair, tissue regeneration, muscle protein synthesis, and gut microbiota modulation across neurodegenerative, cardiovascular, and regenerative disease models.Frontiers in cell and developmental biology · 2026Review
- Bioactive compounds in Chinese herbal medicine: anti-inflammatory mechanisms targeting neurological disorders.Frontiers in nutrition · 2025Review
- UCF-101 ameliorates traumatic brain injury by promoting microglia M2 polarization via AMPK/NF-κB pathways in LPS-induced BV2 cells.Journal of molecular histology · 2024Article
- Tanshinone IIA protects motor neuron-like NSC-34 cells against lipopolysaccharide-induced cell injury by the regulation of the lncRNA TCTN2/miR-125a-5p/DUSP1 axis.Regenerative therapy · 2023Article
- Tanshinone-IIA mediated neuroprotection by modulating neuronal pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Phillyrin Prevents Neuroinflammation-Induced Blood-Brain Barrier Damage Following Traumatic Brain InjuryFrontiers in pharmacology · 2021Article
- Tanshinone IIA Protects Against Cerebral Ischemia Reperfusion Injury by Regulating Microglial Activation and PolarizationFrontiers in pharmacology · 2021Article
- Transplanting Microglia for Treating CNS Injuries and Neurological Diseases and Disorders, and Prospects for Generating Exogenic Microglia.Cell transplantationReview
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeTraumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Increasing evidence indicates that activated microglia play an important role in the inflammatory response in TBI. Inhibiting M1 and stimulating M2 activated microglia have protective effects in several animal models of central nervous system (CNS) disorders. In the present study, we investigated whether tanshinone IIA (TNA) protects neurons by shifting microglia polarization in a mouse TBI model and further investigated the mechanism in vitro. MATERIALS AND
methodsForty C57BL/6 mice were used to investigate the effect of TNA on microglia polarization in TBI. BV-2 cells were used to examine the mechanism of TNA in regulating microglia polarization.
resultsNormal saline (NS), TNA and the combination of TNA with ICI 182,780 (ICI, an estrogen receptor antagonist) were used to treat the TBI mice. After TBI, mice from each group demonstrated functional improvement. The improvement rate in mice treated with TNA was faster than other groups. ICI partially reversed the benefits from TNA treatment. TNA treatment significantly reduced TBI-induced neuronal loss. The number of microglia after TBI was not significantly changed by TNA treatment. However, TNA treatment significantly decreased M1 macrophage markers (iNOS, TNFα and IL-1β) and increased M2 macrophage markers (CD206, arginase 1 and Ym1). This effect was partially abolished by ICI. TNA treatment downregulated M1 macrophage markers and upregulated M2 macrophage markers in BV-2 cells under LPS stimulation. IL-10 was significantly increased by TNA treatment without a significantly change of IL-4 and IL-13 expression. IL-10 knockdown completely abolished the effect of TNA on microglial M2 polarization.
conclusionTaken together, our data demonstrated that TNA attenuates neuronal loss in mouse TBI model and promotes M2 microglia by ERβ/IL-10 pathway. Thus, TNA could be a potential drug for TBI and/or the disorders that caused by microglial over-activation in CNS.
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