ArticleMetabolic brain disease2020
Neuroprotective roles of total flavones of Camellia on early brain injury andcognitive dysfunction following subarachnoid hemorrhage in rats.
Article in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Yucca filamentosa extract therapeutic potential against neuro-inflammation and demyelination through modulation of eicosanoids.Inflammopharmacology · 2026Article
- Dysfunction of hippocampal cells and its role in cognitive impairment.Neural regeneration research · 2026Article
- Article
- Neuroprotective efficacy of 4-Hydroxyisoleucine in experimentally induced intracerebral hemorrhage.Saudi journal of biological sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was undertaken to explore the role of total flavones of Camellia (TFC) on cerebral injury following subarachnoid hemorrhage (SAH) in rats. We showed that the increase of malondialdehyde (MDA) level in brain tissues, leakages of neuron-specifc enolase (NSE) and lactate dehydrogenase (LDH) from brain tissues to serum at 48 h after SAH were significantly blocked by TFC treatment. Besides, TFC treatment could reduce brain edema and the Bax/Bcl-2 ratio in hippocampal tissues at mRNA and protein levels at 48 h after SAH. In addition, and the reduction of neurological scores at 7d after SAH were significantly inhibited by TFC treatment. We next sought to demonstrate the role of TFC on cognitive rehabilitation and the tau phosphorylation in hippocampal tissues at 30d after SAH. Not surprisingly, cognitive dysfunction and the upregulation of tau phosphorylation at Ser262 (p-tau-Ser262) in hippocampal tissues were markedly reduced by TFC treatment. These findings suggested that TFC has protective effect on SAH-induced EBI and subsequent cognitive dysfunction, which may be related to downregulating the Bax/Bcl-2-related apoptosis pathway and inhibition of tau phosphorylation.
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.