ArticleBMC anesthesiology2015
Pretreatment but not subsequent coincubation with midazolam reduces the cytotoxicity of temozolomide in neuroblastoma cells.
Article in BMC anesthesiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Review of the Interactions Between Anesthetic Agents and Chemotherapeutic Agents in Cancer Cell Lines Studied In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Role of midazolam on cancer progression/survival - An updated systematic review.Indian journal of anaesthesia · 2023Article
- Insights into the Roles of Midazolam in Cancer Therapy.Evidence-based complementary and alternative medicine : eCAM · 2017Review
- A narrative review of adjuvant therapy for glioma: hyperbaric oxygen therapy.Medical gas researchReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTemozolomide (TMZ) induces a G2/M cell cycle arrest and is used for treatment of paediatric tumours, especially neuroblastomas. Patients treated with TMZ frequently receive midazolam for sedation prior to surgery and other interventions. Previous studies suggested both cytoprotective and apoptosis-inducing properties of midazolam. Therefore, the impact of midazolam on TMZ-induced cytotoxicity was investigated in vitro.
methodsHuman neuroblastoma cells were incubated with midazolam alone, as a pretreatment prior to incubation with TMZ or a coincubation of both. Cell viability and proliferation was analysed (XTT and BrdU assay) after 24 h and flowcytometric cell cycle analysis was performed after 24 and 48 h.
resultsMidazolam alone increased cell viability at lower concentrations (2, 4, 8, 16 μM), whereas higher concentrations (128, 256, 512 μM) reduced cell viability. Pretreatment with midazolam 6 h prior to TMZ incubation reduced cytotoxic effects (IC25 1005 ± 197 μM; IC50 1676 ± 557 μM; P < 0.05) compared to incubation with TMZ alone (IC25 449 ± 304 μM; IC50 925 ± 196 μM) and reduced the antiproliferative effect of TMZ (1000 μM) by 43.9 % (P < 0.05). In contrast, cytotoxic effects of TMZ were increased (IC75 1175 ± 221 μM vs. 2764 ± 307 μM; P < 0.05) when midazolam pretreatment was followed by coincubation of midazolam and TMZ. Cell cycle analysis revealed increased fractions of cells in G2/M phase after TMZ treatment (100 μM; 48 h), irrespective of midazolam pretreatment.
conclusionMidazolam causes a hormetic dose-response relationship in human neuroblastoma cells. Pretreatment with midazolam reduces the cytotoxic and antiproliferative effects of TMZ without interfering with G2/M cell cycle arrest. In contrast, subsequent midazolam coincubation increases overall cytotoxicity.
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