Validation experiment designed to validate causal mechanisms targeting NFE2L2, HMOX1, TLR4, NFKB1 in streptozotocin-induced diabetic rats. Primary outcome: renal function improvement and reduction in oxidative stress, inflammation, and apoptosis
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.
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.
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.
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
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