Objective

Ischemic stroke, resulting from the interruption of blood supply to the brain, leads to cerebral ischemia, hypoxia, and necrosis, and is a prevalent disease characterized by high incidence, mortality, and disability rates. This study investigates the protective effects of ischelium on cerebral ischemia-reperfusion injury in a rat model, along with the potential mechanisms of action.

Methods

We established a rat cerebral ischemia-reperfusion model and administered different doses of ischelium as intervention across treatment groups. Multiple techniques were used to evaluate brain tissue damage, oxidative stress markers, inflammatory cytokine levels, and apoptosis, while also examining the expression of key proteins in the Nrf2/HO-1 antioxidant pathway and the HMGB1/TLR4/RAGE/NF-κB pro-inflammatory pathway.

Results

The results indicate that ischemia-induced injury causes severe brain tissue damage and activates both the Nrf2/HO-1 antioxidant pathway and the HMGB1/TLR4/RAGE/NF-κB pro-inflammatory pathway, subsequently leading to oxidative stress, inflammation, and apoptosis. Treatment with ischelium significantly alleviated the brain tissue damage induced by cerebral ischemia-reperfusion, promoted the Nrf2/HO-1 antioxidant pathway, and suppressed the HMGB1/TLR4/RAGE/NF-κB inflammatory pathway. Ischelium also reduced MDA levels and increased SOD, CAT, and GSH levels, while inhibiting the production of pro-inflammatory cytokines IL-6, IL-1β, TNF-α and apoptosis.

Conclusions

These findings suggest that ischelium confers neuroprotective effects against cerebral ischemia-reperfusion injury, likely by regulating oxidative stress and neuroinflammation. Further investigations into the exact molecular mechanisms and clinical translations of ischelium may lead to novel therapeutic approaches for ischemic stroke.

Search results

Exploring the protective effects of ischelium on rat brain ischemia-reperfusion injury