ArticleNeurochemical research2026
Melatonin Exerts Neuroprotective Effects in Escherichia coli/Lipopolysaccharide Induced Neuronal Injury via Regulating TFRC-Related Ferroptosis.
Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
Neonatal bacterial meningitis (NBM) is a severe neonatal infectious disease associated with a high incidence of neurological sequelae. Lipopolysaccharide (LPS) and inflammatory cytokines aggravate cerebral injury, whereas the mechanism of ferroptosis in the pathogenesis of NBM remains unclear. Melatonin (MT), an endogenous neurohormone, provides anti-ferroptotic neuroprotection in models of cerebral injury; however, its mechanism of action against NBM-related injury through ferroptosis has not been clarified. This study investigated the protective effects mediated by MT in vivo and in vitro. Rat models of LPS-induced inflammatory brain injury were established through intracerebroventricular (i.c.v.) injection, and Escherichia coli (E. coli)-infected cell models were developed to investigate the neuroprotective effects of MT against TFRC-related ferroptosis. CCK-8 assays, Western blotting, transmission electron microscopy (TEM), iron detection, and immunofluorescence, BODIPY staining were used to assess cell viability, inflammatory factors, mitochondrial ultrastructure, iron accumulation, and GPX4 expression. E. coli infection induced typical ferroptotic mitochondrial damage. MT alleviated neuroinflammation and reduced the expression of ferroptosis-related proteins both in vitro and in vivo. MT treatment increased mitochondrial GPX4 expression. The ferroptosis agonist RSL3 reversed the neuroprotective effects of MT. MT inhibited TFRC-related ferroptosis and alleviated neuronal damage. MT protects against E. coli/Lipopolysaccharide induced neuronal injury by regulating TFRC-related ferroptosis, indicating that MT may be a promising therapeutic agent for NBM.
Indexed as
Identifiers
42873388What 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.