ArticleJournal of cellular and molecular medicine2019
Protein kinase C is involved in the neuroprotective effect of berberine against intrastriatal injection of quinolinic acid-induced biochemical alteration in mice.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Neuroprotective mechanisms of nutraceutical berberine: Preclinical evidence and future perspectives.Advances in neurotoxicology · 2026Article
- Nanomedicine-enabled neuroprotection: therapeutic role of berberine in neurodegenerative diseases.Molecular biology reports · 2025Review
- A critical appraisal on the involvement of plant-based extracts as neuroprotective agents (2012-2022): an effort to ease out decision-making process for researchers.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Berberine hydrochloride improves cognitive deficiency through hippocampal up-regulation of neurotrophins following inhalant self-administration of methamphetamine.Iranian journal of basic medical sciences · 2023Article
- Berberine Ameliorates Subarachnoid Hemorrhage InjuryFrontiers in pharmacology · 2020Article
- Protein kinase C is involved in the neuroprotective effect of berberine against intrastriatal injection of quinolinic acid-induced biochemical alteration in mice.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase C (PKC) shows a neuronal protection effect in neurodegenerative diseases. In this study, we test whether berberine has a positive effect on the activity of PKC in quinolinic acid (QA)-induced neuronal cell death. We used intrastriatal injections of QA mice model to test the effect of berberine on motor and cognitive deficits, and the PKC signalling pathway. Treatment with 50 mg/kg b.w of berberine for 2 weeks significantly prevented QA-induced motor and cognitive impairment and related pathologic changes in the brain. QA inhibited the phosphorylation of PKC and its downstream molecules, GSK-3β, ERK and CREB, enhanced the glutamate level and release of neuroinflammatory cytokines; these effects were attenuated by berberine. We used in vivo infusion of Go6983, a PKC inhibitor to disturb PKC activity in mice brain, and found that the effect of berberine to reverse motor and cognitive deficits was significantly reduced. Moreover, inhibition of PKC also blocked the anti-excitotoxicity effect of berberine, which is induced by glutamate in PC12 cells and BV2 cells, as well as anti-neuroinflammatory effect in LPS-stimulated BV2 cells. Above all, berberine showed neuroprotective effect against QA-induced acute neurotoxicity by activating PKC and its downstream molecules.
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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 Socratic graph.