ArticleBrain and behavior2023
Inhibitory effect and mechanism of Rosiglitazone on M1 type polarization of central microglia in intracerebral hemorrhage mice based on JNK/STAT3 signaling pathway.
Article in Brain and behavior, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Pathological mechanisms and future therapeutic directions of thrombin in intracerebral hemorrhage: a systematic review.Frontiers in pharmacology · 2024Pooled it
- Neurovascular unit remodeling: focusing on glial cells in stroke injury and recovery.Frontiers in cellular neuroscience · 2026Review
- Effects of Lycium barbarum Polysaccharide on Digestive Function and Intestinal Barrier Dysfunction in Septic Mice by Regulating JNK Pathway.Molecular biotechnology · 2025Article
- Emerging Therapeutic Strategies in Intracerebral Hemorrhage: Enhancing Neurogenesis and Functional Recovery.MedComm · 2025Review
- Microglial activation states and their implications for Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2025Review
- Inhibitory effect and mechanism of Rosiglitazone on M1 type polarization of central microglia in intracerebral hemorrhage mice based on JNK/STAT3 signaling pathway.Brain and behavior · 2023Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIntracerebral hemorrhage (ICH) seriously threatens the health of people. In addition, microglia M1 polarization was confirmed to be involved in the progression of ICH. Rosiglitazone was able to be used as an antidiabetic agent, which could activate PPAR-γ, and PPAR-γ was reported to inhibit inflammation in microglia. However, the detailed function of Rosiglitazone in ICH remains unclear.
methodsIn vivo and in vitro experiments were used to test the function of Rosiglitazone in ICH. In addition, RT-qPCR and western blot were performed to evaluate the mRNA and protein level of PPAR-γ, respectively. Immunofluorescence staining was performed to detect the levels of CD206 and CD86, and ELISA was used to measure the levels of pro-inflammatory cytokines.
resultsPPAR-γ was downregulated in ICH mice, whereas p-JNK and p-STAT3 were upregulated. Thrombin notably downregulated the level of PPAR-γ in BV2 cells, whereas Rosiglitazone partially reversed this phenomenon. In addition, Rosiglitazone markedly reversed thrombin-induced microglia M1 polarization. Consistently, thrombin-induced inflammatory response in BV2 cells was abolished in the presence of Rosiglitazone. SP600125 (JNK/STAT3 inhibitor) greatly reversed thrombin-induced M1 polarization in microglia, and GW9662 abolished the effect of SP600125. Meanwhile, Rosiglitazone could inactivate JNK/STAT3 pathway through the upregulation of PPAR-γ. Furthermore, Rosiglitazone notably alleviated the symptom of ICH in vivo through inhibiting the apoptosis and mediating PPAR-γ/JNK/STAT3 axis.
conclusionRosiglitazone could attenuate the inflammation in ICH through inhibiting microglia M1 polarization. Thus, our research would shed now lights on exploring new therapeutic strategies against ICH.
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