Clinical Efficacy Observation And Mechanism Study Of Rt-PA Combined With Edaravone Dexborneol In The Treatment Of Acute Cerebral Infarction

Objective: Acute cerebral infarction is an ischemic disease caused by vascular stenosis or blockage,which can result in a series of problems such as progressive damage to brain tissue and deterioration of neurological function.During acute cerebral infarction,neuronal cells undergo apoptosis due to ischemia and hypoxia,resulting in the accumulation of oxygen free radicals and triggering an inflammatory cascade reaction,which exacerbates brain tissue damage.Recombinant human tissue plasminogen activator(rt-PA)can restore blood supply to ischemic brain tissue by opening blood vessels in the first instance,but its effect is unstable due to various factors.Therefore,it is particularly important to apply other drugs in combination therapy promptly after rt-PA thrombolysis.This study observed changes in the concentrations of pyruvate kinase isozyme type M2(PKM2),high mobility group box 1(HMGB1),interleukin-6(IL-6),toll-like receptor 4(TLR4),matrix metalloproteinase 9(MMP-9),and B-cell lymphoma-2(Bcl-2)in the serum of patients with acute cerebral infarction at different stages.The aim of this study was to investigate the clinical efficacy and mechanism of atorvastatin combined with Edaravone dexborneol in treating acute cerebral infarction.Methods:We selected 60 patients who were admitted to the neurology department of Hebei Medical University Second Hospital for acute ischemic stroke and received atorvastatin thrombolysis treatment from October 2021 to November2022.The eligible subjects were randomly assigned to two groups according to a random number table.The control group received basic treatment for neurology after thrombolysis,including statins and drugs to improve circulation.The experimental group received injection of concentrated solution of Edaravone dexborneol(specifications:Edaravone 10 mg and 2.5mg dexborneol in 5ml solution)and 0.9% sodium chloride injection 100 ml,intravenous infusion twice a day,completed within 30 minutes.The time interval between the two doses was no less than 6 hours,and each cycle lasted12 days.2.The NIHSS and m RS scores were evaluated in both groups on the first day of admission,at 12 days and 3 months of follow-up.We collected 5ml of venous blood from patients before thrombolysis,24 hours after thrombolysis,and on the 12 th day,and used enzyme-linked immunosorbent assay(ELISA)to detect changes in the concentrations of PKM2,HMGB1,IL-6,TLR4,MMP-9,and Bcl-2.Results:Based on the use of idebenone,60 patients were divided into a control group and an experimental group.Based on the experimental results,it was observed that:After one day of medication,the concentrations of the five biomarkers,PKM2,HMGB1,IL-6,TLR4,and MMP9,increased in both groups’ serum.However,the experimental group showed less increase in these biomarkers compared to the control group.Both groups showed a decrease in Bcl-2,but the experimental group showed a smaller decrease.After twelve days,the concentrations of PKM2,HMGB1,and IL-6 in both groups’ serum decreased.However,the experimental group showed a greater decrease in these biomarkers compared to the control group.Both groups showed an increase in TLR4 and MMP9,but the experimental group showed a smaller increase than the control group.Both groups showed a decrease in Bcl-2,but the experimental group showed a smaller decrease.After 12 days of medication,patients in the experimental group showed greater improvement in NIHSS and m RS scores compared to the control group.At the 3-month follow-up,patients in the experimental group continued to show greater improvement in NIHSS and m RS scores compared to the control group.Conclusions:Edaravone dexborneol concentrated solution injection can effectively decrease the concentration of PKM2,HMGB1,and IL-6 in the serum of patients with acute cerebral infarction,inhibit the elevation of TLR4 and MMP-9 concentrations,and suppress the decrease of Bcl-2 concentration,thus improving neurological function deficits and ultimately benefiting patients.Among them,PKM2 and HMGB1 play a significant role in the further development of the condition during the acute phase of cerebral infarction.