🧫
Resveratrol protection against renal I/R injury in diabetic rats
active
experiment
Created: 2026-04-11T00:45:03
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-8b61762b-2663-4111-9e71-d728137b316c
🧫 Experiment Protocol
Validationdiabetic nephropathyNFE2L2, HMOX1, TLR4, NFKB1streptozotocin-induced diabetic ratsproposed
This experiment investigated the protective effects of resveratrol (RSV) against renal ischemia/reperfusion (I/R) injury in streptozotocin-induced diabetic rats. The study examined whether RSV could improve renal function and reduce oxidative stress, inflammatory responses, and apoptosis following I/R injury in diabetic conditions. The mechanism was explored by measuring expression levels of Nrf2, HO-1, TLR4, and NF-κB proteins. To confirm the role of Nrf2 signaling, selective inhibition of Nrf2 was performed using ML385. The diabetic rats were treated with RSV before induction of renal ischemia, and various parameters of kidney injury and molecular markers were assessed after reperfusion.
PRIMARY OUTCOME
renal function improvement and reduction in oxidative stress, inflammation, and apoptosis
EXPECTED OUTCOMES
RSV treatment expected to improve renal function, reduce oxidative stress and inflammation, decrease apoptosis, increase Nrf2/HO-1 expression, and decrease TLR4/NF-κB expression. ML385 treatment expected to abolish RSV benefits.
SUCCESS CRITERIA
Significant improvement in renal function parameters, reduced oxidative stress markers, decreased inflammatory responses and apoptosis, increased Nrf2/HO-1 expression, decreased TLR4/NF-κB expression, and abolishment of benefits with Nrf2 inhibition
PROTOCOL
Streptozotocin induction of diabetes in rats, resveratrol pretreatment, renal ischemia/reperfusion induction, assessment of renal function, oxidative stress markers, inflammatory responses, apoptosis, and protein expression levels of Nrf2, HO-1, TLR4, and NF-κB. Selective Nrf2 inhibition with ML385 to confirm mechanism.
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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