ArticleChinese medicine2021
Scutellarin ameliorates neonatal hypoxic-ischemic encephalopathy associated with GAP43-dependent signaling pathway.
Article in Chinese medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 18 citations in OpenAlex.
- Optogenetic Strategies for Motor Recovery After Ischemic Stroke: Mechanisms and Therapeutic Implications.Cellular and molecular neurobiology · 2026Review
- Scutellarin Modulates Astrocyte-Microglia-Neuron Crosstalk to Mitigate Neuroinflammation and Apoptosis in Cerebral Ischemia.Molecular neurobiology · 2025Article
- miR-758-3p Interferes with Neuronal Apoptosis in Cerebral Ischemia-Reperfusion by Inhibiting ILK.Molecular neurobiology · 2025Article
- An unstable variant of GAP43 leads to neurodevelopmental deficiency.Scientific reports · 2024Article
- Effect of scutellarin on BV-2 microglial-mediated apoptosis in PC12 cells via JAK2/STAT3 signalling pathway.Scientific reports · 2024Article
- Current advances on the therapeutic potential of scutellarin: an updated review.Natural products and bioprospecting · 2024Review
- Scutellarin: pharmacological effects and therapeutic mechanisms in chronic diseases.Frontiers in pharmacology · 2024Review
- Scutellarin attenuates microglia activation in experimentally induced hypoxia-ischemia brain damage by down-regulating miRNA-7036a.Acta biochimica et biophysica Sinica · 2023Article
- Farrerol Alleviates Hypoxic-Ischemic Encephalopathy by Inhibiting Ferroptosis in Neonatal Rats via the Nrf2 Pathway.Physiological research · 2023Article
- Scutellarin Acts via MAPKs Pathway to Promote M2 Polarization of Microglial Cells.Molecular neurobiology · 2023Article
- MicroRNA-582-5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion-induced injury.Immunity, inflammation and disease · 2022Article
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11 authors at 4 institutions in 1 country.
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Abstract
backgroundNeonatal hypoxic-ischemic encephalopathy (HIE) refers to the perinatal asphyxia caused by the cerebral hypoxic-ischemic injury. The current study was aimed at investigating the therapeutic efficacy of Scutellarin (Scu) administration on neurological impairments induced by hypoxic-ischemic injury and exploring the underlying mechanisms.
methodsPrimary cortical neurons were cultured and subjected to oxygen-glucose deprivation (OGD), and then treated with Scu administration. The growth status of neurons was observed by immunofluorescence staining of TUJ1 and TUNEL. Besides, the mRNA level of growth-associated protein 43 (GAP43) in OGD neurons with Scu treatment was detected by quantitative real-time polymerase chain reaction (qRT-PCR). To further verify the role of GAP43 in Scu treatment, GAP43 siRNA and knockout were applied in vitro and in vivo. Moreover, behavioral evaluations were performed to elucidate the function of GAP43 in the Scu-ameliorated long-term neurological impairments caused by HI insult. The underlying biological mechanism of Scu treatment was further elucidated via network pharmacological analysis. Finally, the interactive genes with GAP43 were identified by Gene MANIA and further validated by qRT-PCR.
resultsOur data demonstrated that Scu treatment increased the number of neurons and axon growth, and suppressed cell apoptosis in vitro. And the expression of GAP43 was downregulated after OGD, but reversed by Scu administration. Besides, GAP43 silencing aggravated the Scu-ameliorated neuronal death and axonal damage. Meanwhile, GAP43 knockout enlarged brain infarct area and deteriorated the cognitive and motor dysfunctions of HI rats. Further, network pharmacological analysis revealed the drug targets of Scu participated in such biological processes as neuronal death and regulation of neuronal death, and apoptosis-related pathways. GAP43 exhibited close relationship with PTN, JAK2 and STAT3, and GAP43 silencing upregulated the levels of PTN, JAK2 and STAT3.
conclusionsCollectively, our findings revealed Scu treatment attenuated long-term neurological impairments after HI by suppressing neuronal death and enhancing neurite elongation through GAP43-dependent pathway. The crucial role of Scutellarin in neuroprotection provided a novel possible therapeutic agent for the treatment of neonatal HIE.
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