🧫
Resveratrol effects on HK-2 cells under hypoxia/reoxygenation
active
experiment
Created: 2026-04-11T00:45:03
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-b92b3e79-53a0-47b9-a559-6a9a5a995c13
🧫 Experiment Protocol
Exploratorydiabetic nephropathyNFE2L2, HMOX1, TLR4, NFKB1HK-2 cells cultured in high glucose conditionsproposed
This in vitro experiment complemented the animal study by examining the protective effects of resveratrol on human kidney tubular epithelial cells (HK-2) under conditions mimicking ischemia/reperfusion injury. HK-2 cells were cultured in high glucose conditions to simulate diabetic conditions, then treated with resveratrol before subjecting them to hypoxia/reoxygenation stress. The study likely assessed cell viability, oxidative stress markers, inflammatory responses, apoptosis, and expression of the same molecular targets (Nrf2, HO-1, TLR4, NF-κB) examined in the animal model to validate the proposed mechanism at the cellular level.
PRIMARY OUTCOME
cell protection against hypoxia/reoxygenation injury
EXPECTED OUTCOMES
RSV treatment expected to improve cell viability, reduce oxidative damage and inflammatory responses, decrease apoptosis, and modulate Nrf2/HO-1 and TLR4/NF-κB signaling pathways similar to the animal model results
SUCCESS CRITERIA
Improved cell survival, reduced oxidative stress and inflammation markers, decreased apoptosis, and consistent molecular pathway modulation matching animal model findings
PROTOCOL
HK-2 cell culture in high glucose medium, resveratrol pretreatment, hypoxia/reoxygenation induction, assessment of cell viability, oxidative stress, inflammatory markers, apoptosis, and protein expression levels
LINKED HYPOTHESES
Source: PMID 41958068 ↗
🧫 Experiment Extras
PATHWAY
Nrf2/HO-1 signaling, TLR4/NF-κB pathway, oxidative stress response, inflammation
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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