ArticleNeurochemical research2011
Scutellarin blocks sodium current in freshly isolated mouse hippocampal CA1 neurons.
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Scutellarin as a Potential Therapeutic Agent for Microglia-Mediated Neuroinflammation in Cerebral Ischemia.Neuromolecular medicine · 2016Review
- In vitro inhibitory effects of scutellarin on six human/rat cytochrome P450 enzymes and P-glycoprotein.Molecules (Basel, Switzerland) · 2014Article
- Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with (18) F-Fluorodeoxyglucose MicroPET.Evidence-based complementary and alternative medicine : eCAM · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scutellarin (Scu), the main bioactive component of Erilgeron breviscapus, protects the brain against ischemic damages. To explore the therapeutic mechanism of Scu, we investigated the impact of Scu on sodium current (I(Na)) of freshly isolated mouse hippocampal CA1 neurons using the whole-cell patch clamp technique. Results showed that Scu inhibited I(Na) in concentration- and holding potential-dependent manners. At 50 μM, Scu markedly shifted the steady state inactivation curve of I (Na) towards a more negative potential, slowed down the recovery of I(Na) from inactivation state, and elicited a frequency-dependent block of I (Na). The shape of the current-voltage (I-V) curve and the steady state activation curve of I(Na) were unaffected by Scu treatment. These findings suggest that Scu is capable of inhibiting I(Na) in neurons through predominantly affecting the inactivated state of I(Na). Inhibition of Na(+) channels provides a novel pharmacological basis for the anti-ischemic application of Scu.
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.