Abstract
Ischemic stroke poses a serious threat to human health. Its high morbidity, disability, and lethality rates have led to it being a research hotspot. Cerebral ischemia reperfusion injury is a difficult point in the treatment of ischemic stroke. In recent years, studies have shown that repeated transcranial magnetic stimulation (rTMS) can enhance cerebral ischemic tolerance and have a significant protective effect on reperfusion injury after ischemia, but its specific mechanism is unknown. The Nrf2/pathway plays a vital role in ischemia-reperfusion injury in the body environment. Therefore, in this experiment, the middle cerebral artery occlusion (MCAO) reperfusion model of SD rats was made to simulate the occurrence of experimental cerebral infarction by the suture method. After treatment with rTMS, it was studied whether it can regulate the expression of Nrf2 and HO-1, affect the content of MDA and SOD activity, and then activate the Nrf2 pathway to exert its brain protection. The results showed that after MCAO reperfusion, the neurological deficit score of rats increased, and the time to remove the bilateral stickers and the time to cross the balance beam increased, suggesting the successful establishment of the experimental cerebral infarction model. Detecting the brain tissue of experimental cerebral infarction rats found that the expression of Nrf2 and HO-1 decreased, the content of MDA increased, and the activity of SOD decreased. After rTMS treatment, the neuromotor function of experimental cerebral infarction rats improved, the expression of Nrf2 and HO-1 in the brain tissue gradually increased, the content of MDA decreased, and the activity of SOD increased. It indicates that the expression of Nrf2 and HO-1 in experimental cerebral infarction rats is reduced. After treatment with rTMS, it can improve the neuromotor function damage of the rats and reduce the level of oxidative stress. The mechanism may be through promoting the activation of the Nrf2 signaling pathway, acting on the expression of antioxidant proteins, such as HO-1 and SOD1, reducing oxidative stress damage, and playing a protective effect on brain tissue.
Highlights
Cerebral infarction, known as ischemic stroke, is due to the interruption of blood supply to the brain, resulting in the lack of oxygen and glucose supply in the brain tissue, resulting in focal tissue necrosis and softening
Cerebral infarction refers to ischemic necrosis or softening of brain tissue, leading to cerebral blood circulation disorders and tissue ischemia and hypoxia. e prognosis is good for mild cases and life-threatening in severe cases
It was found that in rats treated with repeated transcranial magnetic stimulation (rTMS), the neurological deficit scores were reduced, and the time to remove bilateral stickers and the time to cross the balance beam was reduced, which confirmed that rTMS can improve the neuromotor function of rats with experimental cerebral infarction. rough observation, we found that the expression of Nuclear transcription factor E2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) protein, and mRNA in the brain tissue of rats in the rTMS treatment group increased, the level of superoxide dismutase (SOD) increased, and the level of MDA decreased
Summary
Known as ischemic stroke, is due to the interruption of blood supply to the brain, resulting in the lack of oxygen and glucose supply in the brain tissue, resulting in focal tissue necrosis and softening. It is characterized by high incidence and high fatalities, disability rate, high recurrence rate, and high fatality rate, and it is becoming younger and younger [1]. E core pathological links of ischemia-reperfusion injury mainly include oxidative stress damage and the chain reaction of free radicals [3]. E large increase in ROS products will aggravate ischemia-reperfusion injury in many ways, including blood-brain barrier destruction, inflammation, and apoptosis. As a natural antioxidant enzyme, superoxide dismutase (SOD) can scavenge ROS in the body, and its activity reflects the body’s ability to scavenge oxygen free radicals [6]
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