Evidence map›Paper›PMID 42886268›Full record

ArticleMolecular biology reports2026

Resveratrol attenuates hydrogen peroxide- and ADP-ribose-associated calcium dysregulation, oxidative stress, and apoptosis in TRPM2-transfected Chinese hamster ovary (CHO)-K1 cells.

Aysun Alparslan Çulha, Esra Nur Tola, Seyit Ali Köse, Abdülhadi Cihangir Uğuz

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Aysun Alparslan ÇulhaDepartment of Obstetrics and Gynecology, Research and Training Center of Başkent University, Konya, Turkey.
Esra Nur TolaDepartment of Obstetrics and Gynecology, Pendik Medipol Hospital, Medipol University, İstanbul, Turkey.
Seyit Ali KöseDepartment of Obstetrics and Gynecology, Akşehir Park Hayat Hospital, Konya, Turkey.
Abdülhadi Cihangir UğuzDepartment of Biophysics, Faculty of Medicine, Karamanoğlu Mehmetbey University, Karaman, Turkey. cihangiruguz@yahoo.com.

Funding

the Scientific Research Projects Coordination Unit of Süleyman Demirel University 4091-TU2-14
6 · The paper itself

Abstract

Oxidative stress can couple reactive oxygen species generation to dysregulated intracellular calcium signaling and apoptosis. This study investigated whether resveratrol modified hydrogen peroxide (H₂O₂)- and adenosine diphosphate ribose (ADPR)-associated cellular injury in transient receptor potential melastatin 2 (TRPM2)-transfected Chinese hamster ovary (CHO)-K1 cells. Cells were assigned to control, resveratrol, H₂O₂, ADPR, H₂O₂ plus resveratrol, and ADPR plus resveratrol groups. H₂O₂ and ADPR increased the integrated Ca²⁺ response, apoptosis, JC-1 fluorescence, caspase activities, intracellular oxidant production, and malondialdehyde, but reduced glutathione and glutathione peroxidase activity (p < 0.05). Resveratrol pretreatment attenuated most of these effects and restored the glutathione and glutathione peroxidase-related antioxidant indices; however, it did not decrease malondialdehyde under the tested conditions, a dissociation that is compatible with the different temporal resolution of the two oxidant readouts used here. These findings indicate that resveratrol modifies several oxidative, calcium-associated, mitochondrial, and apoptotic responses in TRPM2-transfected CHO-K1 cells.

Indexed as

Adenosine Diphosphate RiboseApoptosisCalciumOxidative StressStilbenesTRPM Cation ChannelsAnimalsAntioxidantsCalcium SignalingCHO CellsCricetinaeCricetulusGlutathioneHydrogen PeroxideMalondialdehydeReactive Oxygen SpeciesAdenosine Diphosphate RiboseAntioxidantsCalciumGlutathioneHydrogen PeroxideMalondialdehydeReactive Oxygen SpeciesResveratrolStilbenesTRPM Cation ChannelsADP-riboseApoptosisCalcium signalingChinese hamster ovary cellsOxidative stressResveratrolTRPM2

Identifiers

PMID42886268

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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.