ArticleJournal of molecular neuroscience : MN2018
Clonidine Protects Against Neurotoxicity Induced by Sevoflurane Through NF-κB Signaling Inhibition and Proinflammatory Cytokine Release in Rats.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 12 citations in OpenAlex.
- The Effects of Hesperidin on Neuronal Apoptosis and Cognitive Impairment in the Sevoflurane Anesthetized Rat are Mediated Through the PI3/Akt/PTEN and Nuclear Factor-κB (NF-κB) Signaling Pathways.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure of neonatal animals to anesthetics may cause developmental functional changes and acute structural anomalies in the brain. Clonidine, an α2-adrenoceptor agonist, functions as an analgesic and sedative and protects against brain injury. Nevertheless, whether clonidine protects the developing brain from damage caused by sevoflurane (SEVO) anesthesia remains unclear. Seven-day-old rats were exposed to 3% SEVO for 6 h, during which time either clonidine or saline was injected three times. The arterial blood gases, respiratory rate, and anesthesia level of each rat were evaluated. Western blot analysis was employed to detect proinflammatory cytokines, NF-κB, and cleaved-caspase-3. Surgical anesthesia was adequately induced by SEVO. No rats died during the study. Compared with untreated rats, SEVO induced production of cleaved-caspase-3. Administration of clonidine and SEVO significantly reduced apoptosis. Moreover, nuclear translocation and NF-κB phosphorylation were inhibited by clonidine, and interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) production decreased after SEVO administration. Marked apoptosis in the brain was induced by SEVO anesthesia. Clonidine treatment provided significant protection against SEVO-induced apoptosis.
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.