ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2014
Effects of exposure to high glucose on primary cultured hippocampal neurons: involvement of intracellular ROS accumulation.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 30 citations in OpenAlex.
- Diabetes, prediabetes, and mild cognitive impairment among older adults: the Hitachi Health Study II.Acta diabetologica · 2026Article
- Shichangpu-Xiyangshen Herb Extract Alleviates Cognitive Dysfunction in Type 1 Diabetes Through Metabolism of Arachidonic Acid Cyclooxygenase and Lipoxygenase.Molecules (Basel, Switzerland) · 2026Article
- Targeting p75NTR activity alleviates the neurotoxic effect of high glucose on iPSC-derived dopaminergic neurons.Stem cell research & therapy · 2026Article
- Altered leptin signaling and attenuated cardiac vagal activity in rats with type 2 diabetes.Frontiers in physiology · 2025Article
- Celecoxib ameliorates diabetic neuropathy by decreasing apoptosis and oxidative stress in dorsal root ganglion neurons via the miR-155/COX-2 axis.Experimental and therapeutic medicine · 2021Article
- Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+AβNeurochemistry international · 2020Article
- Brain-derived neurotrophic factor inhibits hyperglycemia-induced apoptosis and downregulation of synaptic plasticity-related proteins in hippocampal neurons via the PI3K/Akt pathway.International journal of molecular medicine · 2019Article
- SDH2 is involved in proper hypha formation and virulence in Candida albicans.Future microbiology · 2018Article
- Characteristic Metabolic Alterations Identified in Primary Neurons Under High Glucose Exposure.Frontiers in cellular neuroscience · 2018Article
- The biochemical alterations underlying post-burn hypermetabolism.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Article
- Activation of mTOR signaling mediates the increased expression of AChE in high glucose condition: in vitro and in vivo evidences.Molecular neurobiology · 2016Article
- Relationship of endothelin-1 and NLRP3 inflammasome activation in HT22 hippocampal cells in diabetes.Life sciences · 2016Article
- bFGF Promotes the Migration of Human Dermal Fibroblasts under Diabetic Conditions through Reactive Oxygen Species Production via the PI3K/Akt-Rac1- JNK Pathways.International journal of biological sciences · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies showed that hyperglycemia is the main trigger of diabetic cognitive impairment and can cause hippocampus abnormalities. The goal of this study is to explore the effects of different concentrations of high glucose for different exposure time on cell viability as well as intracellular reactive oxygen species (ROS) generation of primary cultured hippocampal neurons. Hippocampal neurons were exposed to different concentrations of high glucose (50, 75, 100, 125, and 150 mM) for 24, 48, 72 and 96 h. Cell viability and nuclear morphology were evaluated by MTT and Hoechst assays, respectively. Intracellular ROS were monitored using the fluorescent probe DCFH-DA. The results showed that, compared with control group, the cell viability of all high glucose-treated groups decreased significantly after 72 h and there also was a significant increase of apoptotic nuclei in high glucose-treated groups from 72 to 96 h. Furthermore, 50 mM glucose induced a peak rise in ROS generation at 24 h and the intracellular ROS levels of 50 mM glucose group were significantly higher than the corresponding control group from 6 to 72 h. These results suggest that hippocampal neurons could be injured by high glucose exposure and the neuronal injury induced by high glucose is potentially mediated through intracellular ROS accumulation.
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.