ArticleMolecular medicine reports2018
Anesthetic agent etiomidate induces apoptosis in N2a brain tumor cell line.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Beyond adrenal suppression: a comprehensive post-marketing safety profile of etomidate from real world data.Frontiers in medicine · 2026Article
- Systemic immune effects of anesthetics and their intracellular targets in tumors.Frontiers in medicine · 2022Review
- Etomidate inhibits cell proliferation and induces apoptosis in A549 non-small cell lung cancer cells via downregulating WWP2.Experimental and therapeutic medicine · 2021Article
- Effects of Anesthesia on Postoperative Recurrence and Metastasis of Malignant Tumors.Cancer management and research · 2020Review
- Effect of Propofol and Etomidate on the Proliferation, Cell-cycle Distribution, Apoptosis and Necrosis of Pancreatic Tumour Cells.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study identified the cytotoxic effects of etomidate on the N2a neuroblastoma cell line. Etomidate induced apoptosis in N2a cells in a concentration‑dependent manner, which was confirmed by western blotting and flow cytometry. Phase contrast microscopy was used to analyze the effect of etomidate on morphological characteristics. The number of the apoptotic cells was increased and confirmed by DAPI and PI staining, which served as a characteristic hallmark of apoptosis. Additionally, etomidate led to loss of mitochondrial membrane potential and resulted in the generation of reactive oxygen species in N2a cells. The western blot analysis revealed that N2a cells treated with etomidate had a significant modulation of pro‑apoptotic proteins, includingpoly ADP‑ribose polymerase (PARP), cleaved PARP, caspase‑9 and procaspase‑3. In conclusion, the present study determined that etomidate induced cytotoxic and apoptotic effects in N2a brain tumor cells in vitro.
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Registered trials
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