Description

Acute cerebral infarction is an ischemic disease caused by the narrowing or blockage of cerebral blood vessels, which can lead to a series of complications such as progressive brain tissue damage and deterioration of neurological function. According to epidemiological surveys, acute cerebral infarction is the second deadliest disease in the world, with a rapid onset, rapid progression, high disability rate, and high mortality rate. In clinical work, it was found that many patients with acute cerebral infarction experienced a further exacerbation of symptoms; this is clinically known as a progressive stroke. The progressive stroke is a type of cerebral infarction in which the neurological impairment is progressively aggravated after the onset of the disease or after clinical treatment. Patients and their families are often unable to understand and accept such changes in their condition, and therefore, effectively blocking the progression of the acute-phase of cerebral infarction has become one of the most problematic situations during the course of clinical treatment.

Currently, the clinically preferred treatment option for patients with acute cerebral infarction is revascularization therapy, in which rt-PA can open the blood vessels at the first time to restore the blood supply to ischemic brain tissues. However, the effect of rt-PA thrombolysis decreases with the passage of the time from drug application, which often leads to a low rate of recanalization as well as other uncertainties. Only a few patients are benefited, and the condition in a small number of patients does not improve significantly after thrombolysis, and disease even progresses. Therefore, the timely application of other drugs after thrombolysis is particularly important.

The pathogenesis of cerebral infarction has not yet been fully elucidated. However, the mechanisms of carotid atheromatous plaque formation, oxidative stress, and inflammation are widely recognized, and the above mechanisms are interconnected. Studies have shown that after acute cerebral infarction, neuronal cells may suffer from ischemia and hypoxia, leading to apoptosis and a large accumulation of reactive oxygen species, which triggers an immunoinflammatory response and exacerbates brain tissue damage. Brain tissue damage will be exacerbated by the immunoinflammatory response. Recent studies have also found that abnormal glucose metabolism plays a crucial role in the pathogenesis of acute cerebral infarction, and that abnormal glucose metabolism accelerates the course of disease, promoting the production of inflammation, reactive oxygen species (ROS), and other substances, which affects disease progression.

The edaravone dexborneol Concentrated Solution for Injection is composed of edaravone and dexborneol in a 4:1 ratio. Edaravone is a free radical scavenger and can effectively remove the accumulation of free radicals after acute cerebral infarction, impede disease progression, and improve the prognosis of cerebral infarction. Dexborneol is a naturally occurring terpene bicyclic organic compound. Dexborneol is anti-inflammatory and can effectively inhibit inflammatory cytokines. The combination of both of them can cut off the pathway between the free radicals and the inflammation, and effectively prevents the disease progression caused by the oxidative stress and inflammation that otherwise leads to disease development.

The timely use of drugs after thrombolysis can effectively improve patients' neurological impairment. Therefore, we explored the clinical efficacy of rt-PA combined with edaravone and dexborneol for the treatment of acute cerebral infarction, to clarify whether their combined use could improve cerebral blood supply of patients through the reconstruction of the blood. This study also sought to determine the mechanism of action of edaravone and dexborneol to guide the selection of therapies for cerebral infarction and improve the patient outcomes.