ArticleMetabolic brain disease2023
Regulation of oxygen-glucose deprivation/reperfusion-induced inflammatory responses and M1-M2 phenotype switch of BV2 microglia by lobetyolin.
Article in Metabolic brain disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Neuroprotective Effects of Furanoditerpenes fromACS chemical neuroscience · 2026Article
- Lobetyolin reshapes gut microbiota and bile acid metabolism to improve androgen-driven PCOS phenotypes in mice.Frontiers in microbiology · 2026Article
- (Ba,Ca)(Ti,Sn)OFrontiers in cellular neuroscience · 2026Article
- Mechanisms of action of retinal microglia in diabetic retinopathy (Review).International journal of molecular medicine · 2025Review
- Lobetyolin, an anti-AD factor from the diet campanulaceae source, metabolism regulation and target exploration.Natural products and bioprospecting · 2025Article
- Lobetyolin alleviates IMQ‑induced psoriasis‑like skin inflammation by maintaining the homeostasis of the skin and inhibiting the inflammatory cytokines in dendritic cells.International journal of molecular medicine · 2025Article
- TREM2-mediated regulation of microglial activity: a promising target for the treatment of ischemic stroke.Journal of translational medicine · 2025Review
- Chemokines-like factor 1 as a serological biomarker in relation to disease severity and 90-day prognosis after spontaneous intracerebral hemorrhage: a prospective cohort study.Neurosurgical review · 2025Article
- Sulfasalazine improves neuronal function in mice with ischemic stroke by inhibiting the STING/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Lobetyolin Suppressed Osteoclastogenesis and Alleviated Bone Loss in Ovariectomy-Induced Osteoporosis via Hindering p50/p65 Nuclear Translocation and Downstream NFATc1/c-Fos Expression.Drug design, development and therapy · 2025Article
- Oxygen Glucose Deprivation-Induced Lactylation of H3K9 Contributes to M1 Polarization and Inflammation of Microglia Through TNF Pathway.Biomedicines · 2024Article
- Lobetyolin protects mice against LPS-induced sepsis by downregulating the production of inflammatory cytokines in macrophage.Frontiers in pharmacology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To elucidate the protective mechanism of lobetyolin on oxygen-glucose deprivation/reperfusion (OGD/R)-induced damage in BV2 microglial cells. The OGD/R model was established using a chemical modeling method to simulate in vivo brain ischemia in lobetyolin-pretreated BV2 cells. The optimum lobetyolin dosage, chemical concentration, and OGD/R modeling duration were screened. The changes in cell morphology were observed, and the levels of immune response-related factors, including tumor necrosis factor-α (TNF-α), interleukin-6, inducible nitric oxide synthase (iNOS), and cluster of differentiation (CD)206, were detected using the enzyme-linked immunosorbent assay. The expression of chemokine-like-factor-1 (CKLF1), hypoxia-inducible factor (HIF)-1α, TNF-α, and CD206, was detected using western blotting. The gene expression of M1 and M2 BV2 phenotype markers was assessed using quantitative polymerase chain reaction (qPCR). The localization of M1 and M2 BV2 markers was detected using immunofluorescence analysis. The results showed that lobetyolin could protect BV2 cells from OGD/R-induced damage. After OGD/R, CKLF1/C-C chemokine receptor type 4 (CCR4) levels increased in BV2 cells, whereas the CKLF1/CCR4 level was decreased due to lobetyolin pretreatment. Additionally, BV2 cells injured with OGD/R tended to be M1 type, but lobetyolin treatment shifted the phenotype of BV2 cells from M1 type to M2 type. Lobetyolin decreased the expression of TNF-α and HIF-1α but increased the expression of transforming growth factor-β (TGF-β) in BV2 cells, indicating a dose-effect relationship. The qPCR results showed that lobetyolin decreased the expression of CD16, CD32, and iNOS at the gene level and increased the expression of C-C-chemokine ligand-22 and TGF-β. The immunofluorescence analysis showed that lobetyolin decreased CD16/CD32 levels and increased CD206 levels. Lobetyolin can protect BV2 cells from OGD/R-induced damage by regulating the phenotypic polarization of BV2 and decreasing inflammatory responses. Additionally, CKLF1/CCR4 may participate in regulating lobetyolin-induced polarization of BV2 cells via the HIF-1α pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.