Abstract

Background/aims: The paper aimed to investigate the effects of Stigmasterol on inflammatory factors, antioxidant capacity, and apoptotic signaling pathways in brain tissue of rats with cerebral ischemia/reperfusion (I/R) injury. Methods: The neurological deficits of the rats were analyzed and HE staining was performed. The cerebral infarct volume was calculated by means of TTC staining, and neuronal apoptosis was detected by TUNEL staining. At the same time, the contents of glutathione peroxidase, glutathione, superoxide dismutase (SOD), nitric oxide, and malondialdehyde in brain tissue were measured. The expression of the relevant protein was detected by means of Western blotting. Results: The results showed that the neurological deficit score and infarct area of the I/R rats in the soy sterol treatment group were significantly lower than those in the I/R group. Moreover, the levels of carbon monoxide and malondialdehyde in the soysterol group were significantly lower than those in the I/R group, and the expressions of cyclooxygenase-2 (Cox-2) and NF-κB (p65) in the soysterol group were also significantly lower than those in the I/R group. The expression of Nrf2 (nucleus) and heme oxygenase-1 (HO-1) increased significantly, and the activities of antioxidant enzymes and SOD were increased. In addition, the stigmasterol treatment can inhibit apoptosis, down-regulate Bax and cleaved caspase-3 expression, and up-regulate Bcl-Xl expression. Conclusion: Stigmasterol protects the brain from brain I/R damage by reducing oxidative stress and inflammation.

Highlights

  • Cerebrovascular disease has become an important disease causing death, with high morbidity, mortality, and disability [1,2]

  • Cerebral infarction refers to the supply of blood flow to the brain caused by various causes, causing irreversible damage to the brain tissue

  • It leads to ischemia and hypoxic necrosis of the brain tissue, which is a common hazard to human health

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Summary

Introduction

Cerebrovascular disease has become an important disease causing death, with high morbidity, mortality, and disability [1,2]. Cerebral infarction refers to the supply of blood flow to the brain caused by various causes, causing irreversible damage to the brain tissue. It leads to ischemia and hypoxic necrosis of the brain tissue, which is a common hazard to human health. The reduction in cerebral blood flow is the most common cause of irreversible brain damage [3]. Studies have found that recovery of blood flow after ischemia can lead to further tissue damage and dysfunction in some cases. This regenerative condition after restoring blood perfusion is called ischemia/reperfusion (I/R) injury.

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