ArticleMolecular neurobiology2025
Neuroprotective Effect of Salvianolic Acid C in Neonatal Rats Following Hypoxic-ischemic Brain Damage.
Article in Molecular neurobiology, 2025. 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.
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- The "habitat-phytochemistry-pharmacological effect" nexus: a multidimensional review of ethnomedicinalFrontiers in pharmacology · 2026Review
- Impact of SARS-CoV-2 variants and vaccination on pediatric febrile seizures: a retrospective cohort study.BMC pediatrics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal hypoxia-ischemia (HI) is a significant cause of lasting disabilities and death in newborns. Salvianolic acid C (SAC), a phenolic compound extracted from Salvia miltiorrhiza, exhibits neuroprotection. However, it is currently uncertain if SAC displays a neuroprotective impact against neonatal hypoxic-ischemic brain damage (HIBD), and if it does, what mechanism is involved. Here, our study found SAC administration (15 mg/kg/day, i.p.) improved muscle strength, motor function, and spatial memory impairment in rats with HIBD. The amelioration of these behaviors was attributed to a notable suppression of neuron loss by SAC in the CA1 and CA3 hippocampal zones. Moreover, oxidative stress analysis revealed SAC enhanced anti-oxidants production while reducing pro-oxidants production. Western blot assays revealed SAC downregulated the levels of phospho-c-Jun N-terminal kinase (p-JNK) and jun proto-oncogene (c-JUN). ELISA measurements further showed SAC effectively diminished pro-inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Collectively, these results suggest SAC exhibits a potential neuroprotective impact by attenuating neuronal injury through inhibiting oxidative stress, JNK pathway activation, and inflammation, thereupon then polishes up motor and cognitive deficits caused by HI in the neonatal rats, indicating SAC may be a promising treatment for neonatal hypoxic-ischemic encephalopathy (HIE).
Indexed as
Identifiers
40522382What Socratic 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 Socratic graph.