| Background:Current studies have shown that acute ischemic stroke(acute cerebral infarction)is the most common of all stroke types,accounting for 60%-80%[1]of all strokes.Severe cerebral infarction is the most difficult type of treatment for the worst prognosis,accounting for 10.3%-25%.What is even more frightening is that the mortality rate is as high as 40%-80%,and it is still as high as 20%-30%[1]after treatment,which brings great burden to the society.However,its research progress is significantly delayed compared to light and medium stroke.In the early stage of acute cerebral infarction,nerve cells are degenerated and necrotic due to ischemia and hypoxia,eventually leading to impaired neurological function.In recent years,domestic and foreign studies have found that a variety of inflammatory markers play a key role in the development of brain edema in acute cerebral infarction.High mobility group protein(HMGB1)and Toll like receptor(TLR4)are related inflammatory markers and play a very important role in the development of brain edema in the early stage of cerebral infarction([2][3].At present,a large number of studies are mainly on the significance of HMGB1 or TLR4 single inflammatory factors and downstream pathway inflammatory factors in acute ischemic stroke.The HMGB1/TLR4 inflammatory pathway is involved in the development and progression of brain edema in patients with severe cerebral infarction.The study of meaning and function has not been reported yet.Objective:This study was to investigate the expression of inflammatory factors HMGB1 and TLR4 in cerebral edema in patients with severe cerebral infarction and its correlation with the occurrence and development of cerebral edema in patients.Method:1.Test subjects:From January 2017 to October 2018,78 patients with acute cerebral infarction admitted to our department of neurology and geriatrics were included in the study.Divided into severe and non-severe groups.1.1.Inclusion criteria:1)Meet the diagnostic criteria for acute cerebral infarction in the Guidelines for the Diagnosis and Treatment of Acute Ischemic Stroke in China 2014.2)Age≧18 years old.3)Onset to 7 days after admission.4)The diagnostic criteria for severe cerebral infarction are as follows(at least one of them):a.NIHSS≥ 15 points:or GCS ≤8 points;b.With tracheal intubation and/or mechanical ventilation;c.Hemodynamic instability;d.Comprehensive tonic-clonic seizures and/or status epilepticus;e.Systemic organ dysfunction requiring supportive care;5)Diagnostic criteria for large-area cerebral infarction are as follows(at least one of them):a.Admitted to hospital CT the following imaging findings:low-density shadows over 50%of the middle cerebral artery region or more than 1/3 of the cerebral hemisphere within 6 hours;or multiple vascular distribution areas;or cerebellar infarction with placeholder effect.b.Admission MRI meets the following imaging findings:large area hemisphere infarct volume exceeds 145 cm3.1.2.Critical group:in accordance with the inclusion criteria 1)-4),1)-3)+(5),1)-5).1.3.Non-severe group:as a control group:patients with cerebral infarction who met the inclusion criteria 1)-3)and did not meet the inclusion criteria 4)and5).2.Specimen collection:8 ml of venous blood sample was taken within 7 days after the onset of the disease.The specimen was centrifuged at 1000Xg for 15 minutes within 30 minutes after collection.The plasma was taken and stored in a refrigerator at 80℃.It is mainly used to determine the expression levels of key inflammatory factors in plasma HMGB1 and TLR4.3.The degree of cerebral infarction edema determination:This study mainly collected the infarct volume and relative signal intensity ratio of the flair and DWI sequences in the head MRI within 7 days of the patient’s onset to quantitatively analyze the degree of cerebral edema in the patient.Result:1.A total of 78 patients with acute cerebral infarction were included in the study,including 38 patients in the severe group and 40 patients in the non-severe group.There was no significant difference in gender,age,hypertension,and diabetes between the two groups(p>0.05).2.The expression levels of HMGB1 and TLR4 in plasma in the severe group were significantly higher than those in the non-severe group.There was significant difference in HMGB1 concentration between the two groups(t=14.740,P<0.05).There was significant difference in TLR4 concentration between the two groups(t=7.832,P<0.05).3.In the FLAIR and DWI sequences,the infarct volume in the severe group was significantly higher than that in the non-severe group.The difference was statistically significant(t=6.220,5.962,both P=0.000);the relative signal intensity ratio of the severe group in the FLAIR and DWI sequences(SIR was significantly more enhanced than non-severe group,and the difference was statistically significant(t=16.634,13.183,both P=0.000).4.The concentration of HMGB1 in plasma was positively correlated with the volume of cerebral infarction in FLAIR and DWI(r=0.545,0.660,P=0.000).The concentration of TLR4 in plasma was positively correlated with the volume of cerebral infarction in FLAIR and DWI(r=0.470,0.449,P=0.000).5.The concentration of HMGB1 in plasma was positively correlated with SIR in FLAIR and DWI sequences(r=0.767,0.665,P=0.000).The concentration of TLR4 in plasma was positively correlated with SIR in FLAIR and DWI sequences(r=0.620,0.553,Both P=0.000).Conclusion:1.The expression levels of plasma HMGB1 and TLR4 in patients with severe cerebral infarction are related to the severity of the disease,which may be independent risk factors.2.The expression levels of HMGB 1 and TLR4 are positively correlated with infarct volume and sir in patients with severe cerebral infarction,so it is closely related to the degree of brain tissue edema.3.Therefore,HMGB1/TLR4 inflammatory pathway is involved in the occurrence and development of brain edema in patients with acute cerebral infarction.May be one of its pathogenesis. |
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