We are analyzing https://link.springer.com/article/10.1007/s00210-025-04079-x.

Title:
Geniposide protects against cerebral ischemic injury by targeting SOX2/RIPK1 axis | Naunyn-Schmiedeberg's Archives of Pharmacology
Description:
Convincing evidence has indicated that geniposide possesses neuroprotective effects in ischemic stroke. This study is designed to explore the potential molecular mechanism of geniposide in oxygen–glucose deprivation/reoxygenation (OGD/R)-treated BV-2 microglial cells and middle cerebral artery occlusion (MCAO) mice. OGD/R model in BV2 microglial cells was established in this research. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8) and flow cytometry assays. Protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), microtubule-associated protein light chain 3 (LC3)-II/LC3-I, Beclin-1, inducible nitric oxide synthase (iNOS), CD86, sex determining region Y-box 2 (SOX2), receptor-interacting serine/threonine-protein kinase 1 (RIPK1), TNF-α, IL-1β, ARG1, and CD163 were detected by western blot assay. RIPK1 mRNA level was determined using real-time quantitative polymerase chain reaction (RT-qPCR). TNF-α and IL-1β levels were analyzed using ELISA kits. After JASPAR analysis, binding between SOX2 and RIPK1 promoter was predicted and verified using chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. The effects of geniposide on cerebral ischemic injury were assessed using MCAO mice in vivo. Geniposide treatment relieved OGD/R-triggered BV-2 cell viability promotion and apoptosis, autophagy, inflammatory response, and M1 polarization inhibition in vitro. SOX2 and RIPK1 expression was decreased in OGD/R-treated BV-2 cells. In mechanism, SOX2 upregulated RIPK1 transcription by binding to the RIPK1 promoter region. Geniposide administration significantly alleviated cerebral ischemic injury in MCAO mice in vivo. Geniposide administration protects against cerebral ischemic injury through regulating the SOX2/RIPK1 axis, providing a potential direction for the application of geniposide in the treatment of ischemic stroke.
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Keywords {🔍}

pubmed, article, google, scholar, cas, geniposide, zhang, stroke, ischemic, central, cell, cerebral, liu, cells, ripk, sox, injury, wang, transcription, μgml, ogdr, factors, data, research, effects, pathway, httpsdoiorgs, axis, microglia, ischemia, signaling, int, httpsdoiorg, biol, privacy, cookies, content, analysis, information, viability, inflammatory, polarization, access, activation, med, drug, ding, neurosci, authors, kunshan,

Topics {✒️}

lncrna pvt1/microrna-24-3p/stat3 axis ripk1-mediated ripk3/mlkl signaling ogd/r-treated bv-2 cells ogd/r-induced bv2 cells nf-κb signaling pathway month download article/chapter nlrp3 inflammasome-related-inflammation akt/nrf2 pathway d-galactose/ovariectomized alzheimer mir-342-5p/acsl4 axis oxygen–glucose deprivation/reoxygenation oxygen-glucose deprivation/reoxygenation ogd/r-treated microglia oxygen-glucose deprivation/reperfusion targeting sox2/ripk1 axis dual-luciferase reporter assays gene-set enrichment analysis article naunyn-schmiedeberg' integrative pharmacology-based analysis full article pdf modulating microglia/macrophage polarization hif-1α signaling kinase-2 catalytic domain human transcription factors privacy choices/manage cookies holmes ze hamilton dj dna-binding specificity overdose-induced hepatotoxicity bv2 microglial cells ya li plotted renal ischemia reperfusion bv2 cells treated sox2/ripk1 axis necrostatin-1 prevents necroptosis geniposide administration protects pask-eef1a1 axis transcription factor eb anti-inflammatory phenotype stat3 pathway measure cell viability limit cell death cerebral ischemic injury high resolution image normal bv2 cells cerebral ischemia injury chunyang xu performed inflammatory response access cerebral ischemic/reperfusion cerebral ischemia reperfusion

Schema {🗺️}

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         headline:Geniposide protects against cerebral ischemic injury by targeting SOX2/RIPK1 axis
         description:Convincing evidence has indicated that geniposide possesses neuroprotective effects in ischemic stroke. This study is designed to explore the potential molecular mechanism of geniposide in oxygen–glucose deprivation/reoxygenation (OGD/R)-treated BV-2 microglial cells and middle cerebral artery occlusion (MCAO) mice. OGD/R model in BV2 microglial cells was established in this research. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8) and flow cytometry assays. Protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), microtubule-associated protein light chain 3 (LC3)-II/LC3-I, Beclin-1, inducible nitric oxide synthase (iNOS), CD86, sex determining region Y-box 2 (SOX2), receptor-interacting serine/threonine-protein kinase 1 (RIPK1), TNF-α, IL-1β, ARG1, and CD163 were detected by western blot assay. RIPK1 mRNA level was determined using real-time quantitative polymerase chain reaction (RT-qPCR). TNF-α and IL-1β levels were analyzed using ELISA kits. After JASPAR analysis, binding between SOX2 and RIPK1 promoter was predicted and verified using chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. The effects of geniposide on cerebral ischemic injury were assessed using MCAO mice in vivo. Geniposide treatment relieved OGD/R-triggered BV-2 cell viability promotion and apoptosis, autophagy, inflammatory response, and M1 polarization inhibition in vitro. SOX2 and RIPK1 expression was decreased in OGD/R-treated BV-2 cells. In mechanism, SOX2 upregulated RIPK1 transcription by binding to the RIPK1 promoter region. Geniposide administration significantly alleviated cerebral ischemic injury in MCAO mice in vivo. Geniposide administration protects against cerebral ischemic injury through regulating the SOX2/RIPK1 axis, providing a potential direction for the application of geniposide in the treatment of ischemic stroke.
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      description:Convincing evidence has indicated that geniposide possesses neuroprotective effects in ischemic stroke. This study is designed to explore the potential molecular mechanism of geniposide in oxygen–glucose deprivation/reoxygenation (OGD/R)-treated BV-2 microglial cells and middle cerebral artery occlusion (MCAO) mice. OGD/R model in BV2 microglial cells was established in this research. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8) and flow cytometry assays. Protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), microtubule-associated protein light chain 3 (LC3)-II/LC3-I, Beclin-1, inducible nitric oxide synthase (iNOS), CD86, sex determining region Y-box 2 (SOX2), receptor-interacting serine/threonine-protein kinase 1 (RIPK1), TNF-α, IL-1β, ARG1, and CD163 were detected by western blot assay. RIPK1 mRNA level was determined using real-time quantitative polymerase chain reaction (RT-qPCR). TNF-α and IL-1β levels were analyzed using ELISA kits. After JASPAR analysis, binding between SOX2 and RIPK1 promoter was predicted and verified using chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. The effects of geniposide on cerebral ischemic injury were assessed using MCAO mice in vivo. Geniposide treatment relieved OGD/R-triggered BV-2 cell viability promotion and apoptosis, autophagy, inflammatory response, and M1 polarization inhibition in vitro. SOX2 and RIPK1 expression was decreased in OGD/R-treated BV-2 cells. In mechanism, SOX2 upregulated RIPK1 transcription by binding to the RIPK1 promoter region. Geniposide administration significantly alleviated cerebral ischemic injury in MCAO mice in vivo. Geniposide administration protects against cerebral ischemic injury through regulating the SOX2/RIPK1 axis, providing a potential direction for the application of geniposide in the treatment of ischemic stroke.
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