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Objective To explore the effect of Kaolin combined with propranolol on matrix metalloproteinase-9 (MMP-9) in lungs of paraquate (PQ) intoxicated mice and the mechanism of protection for lung injury. Methods Fifty-four ICR mice were randomly divided into three groups, 18 mice in each group: namely control group, PQ intoxicated group and treatment group. The PQ intoxicated model was replicated by intra-gastric administration (ig) of PQ 100 mg/kg; after intoxication, 48 g/kg Kaolin combined with 3.2 mg/kg propranolol intra-gastric administration was immediately given to the treatment group, while in the control group, the same volume of normal saline ig was applied. All the mice were sacrificed at 6, 12 and 24 hours after disposal, and the lung was harvested to test the protein expression level of MMP-9 by Western Blot, and the lung tissue pathological changes were observed.Results There was no statistical significance in the protein expression levels of MMP-9 among the control group, PQ intoxicated group and treatment group at 6 hours after disposal (grey value: 0.655±0.045, 0.656±0.045, 0.641±0.036). The protein expression levels of MMP-9 in PQ intoxicated group were increased significantly compared with those in the control group at 12 hours and 24 hours after disposal (12 hours: 0.824±0.039 vs. 0.634±0.038, 24 hours: 0.742±0.039 vs. 0.658±0.041, bothP < 0.05), while the levels of treatment group were significantly lower than those in the intoxicated group (12 hours: 0.760±0.050 vs. 0.824±0.039, 24 hours: 0.686±0.041 vs. 0.742±0.039, bothP < 0.05). In PQ intoxicated group, early capillary dilation and congestion in lung tissue, a large number of inflammatory cells infiltration with mainly neutrophils in alveolar cavity and a small number of red blood cells exudation were seen at 12 hours; at 24 hours, capillary dilation at alveolar walls, congestion, swelling of endothelial cells, small flakes or large patches of inflammatory cell infiltration with mainly neutrophils in lungs were found. In the treatment group, the lung inflammatory cells infiltration, alveolar capillary dilatation, congestion, swelling of the endothelial cells, etc were also visible, but the degree of severity was significantly milder than those in the intoxicated group.Conclusion The interference of Kaolin combined with propranolol can significantly decrease the protein expression level of MMP-9 in lung tissue of acute paraquat poisoned mice that is possibly one of the mechanisms for prevention and treatment of lung injury in paraquat poisoning.
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Objective To observe the change and its clinical significance of serum B-type brain natriuretic peptide (BNP) concentration in patients with acute cerebral hemorrhage. Methods The plasma BNP level was measured by microparticle enzyme immunosorbent assay (MEIA) method in 100 patients with acute cerebral hemorrhage. The blood volume of cerebral hemorrhage was computed respectively. The Glasgow Coma Scale (GCS) and National Institutes of Health Stroke Scale (NIHSS) were used to evaluate nerve function on the 1st, 3rd, 7th and 15th day after admission, and the Glasgow Out-come Scale (GOS) was used when the patient was discharged from hospital or died. Results The plasma BNP level at the 2nd day after admission was positively correlated with the blood volume of cerebral hemorrhage in patients with acute cerebral hemorrhage (r=0.367, P=0.000), with NIHSS score at the 1st, 3rd, 7th and 15th after admission (r=0.491, 0.444, 0.427 and 0.458, all P=0.000), and with GOS score (r=0.507, P=0.000). In addition, it was negatively correlated with GCS score at the 1st, 3rd, 7th and 15th after admission (r=-0.553, -0.429, -0.473 and -0.501, all P=0.000). Conclusions The plasma level of BNP is good for predicting the strike of cerebral hemorrhage patient′s condition, it is likely to provide a original thread for judge the severe degree of patient′s condition.
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Objective To observe the effect on succinate dehydrogenase (SDH) of mitochondria in myocardium and liver in sepsis rats treated with edaravone. Methods 30 Sprague-Dawley rats were divided into 3 groups: sham operated group ( group A ), controlled operated group ( group B ), treated group with edaravone (group C). The model of sepsis rats was made by the way of caecum ligated and punctured and 20mg/kg lactate levofloxacin was subcutaneously injected (sci) 15min before and 3h after operation in three group. 5mg/kg edaravone were sci 15min before and 3h after operation in group C. Liver and myocardium were taken from all of them 18h after operation. The activities of SDH in myocardial and hepatic mitochondria were detected, pathological change of mitochondria in liver and myocardium were observed. Results The activities of SDH in myocardial and hepatic mitochondria in group B [ (0. 21 ± 0. 07 ) U/mgprot, (0. 23± 0. 08 ) U/mgprot ] were significantly decreased compared with group A [ ( 0. 33 ± 0. 10 ) U/mgprot, ( 0. 38±0. 12)U/mgprot]. The activities of those in group C[ (0.31 ±0. 08) U/mgprot, (0. 36 ±0. 11)U/mgprot] were significantly increased than group B. Myocardial and hepatic mitochondria swelling and endocytoplasmic reticulum expanding were found in group B by electron microscope, while it showed normal in group C. Conclusion Hepatic and myocardial mitochondrial structure were destroyed and activities of SDH were decreased in sepsis rats. They could be effectively protected by edaravone.
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Objective To analyse correlated risk factors of evolving cerebral infarction(ECI).Methods The follow data was recorded in the acute cerebral infarction (ACI)cases when they were admitted :sex,age,systolic blood pressure(SBP),diastolic blood pressure(DBP),history of disease (diabetes mellitus,hypertension,hyperlipidaemia,cerebral infarction,hyperuricemia or smoking).The following examinations or determinations were done,including:white blood cell count (WBC),platelet count (PLT),blood gluconate(GLU),PT-INR,fibrinogen(FG),TT-INR,APTT-INR,C-reactive protein(CRP),D-dimer(D-D),products of fibrin degradation(FDP),anti-thrombin Ⅲ(ATⅢ),apolipoprotein A(apoA),apolipoprotein B(apoB),blood urea nitrogen(BUN),creatinine(CR),triglyceride (TG),high density lipoprotein (HDL),low density lipoprotein (LDL),very low density lipoprotein (VLDL),GOT,lactate dehydrogenase(LDH),creatine phosphokinase (CPK),MB isoforms of creatine phosphokinase (CPK-MB),? hydroxybutyrate dehydrogenase (?-HBDH),troponin I(TnI),cerebral CT or MRI and carotid ultrasonography.The patients were divided into two groups,ECI and completed cerebral infarction (CCI),according whether neurons function scale deteriorated.When cases of both groups exceeded 50,we took statistic test by SPSS10.0 statistic software.Results 8 of the above 46 markers had significant defference between the two groups,including CRP,WBC,apoB,GLU,LDH,CPK-MB,?-HBDH and DBP.ECI was more common in patients who had lower DBP or higher CRP,WBC,apoB,GLU,LDH,CPK-MB,?-HBDH when they were admitted.Conclusion The increase of CRP,WBC,apoB,GLU,LDH,CPK-MB,?-HBDH or decrease of DBP when patients are admitted can be predictive markers of ECI.