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Objective To investigate the CR low dose radiography to COPD in patients with pseudo normal phenomenon.Methods 160 cases of COPD diagnosed,stratified random dividing method according to the pulmonary function test values were divided into A,B,C and D group.Each group had 32 cases,at the same time,the increase in lung function in patients with mild to moderate pulmonary emphysema in 32 cases was E group,wich was treated with normal dose as a control group,in the normal dose and low dose CR photography failed to clear the diagnosis of emphysema,causing false normalization,statistical the case number,and verify the pulmonary function classification criteria,identify false normalization of lesions in such a case,the general rule to judge the feasibility analysis and prevention.Results There was no significant chifference among 5 groups of pseudo normal comparison (x2 =4.56,P ＞0.05).Conclusion Chronic obstructive pulmonary disease with low dose CR photography on severe and extremely severe patients is deteded by emphysema detection with rate high.Moderate,mild COPD detection rate is extremely low.
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Objective To explore the optimum dose of multislice spiral CT scan in the check of patients with chronic obstructive pulmonary disease(COPD).Methods 90 COPD patients were divided into the conventional dose group and low dose group,the quality of conventional-dose and low-dose scan was analyzed respectively.Results The two scanning methods enable images satisfactory requirements in the 90 cases,and low-dose CT radiation dose was significantly reduced(t=5.01,6.82,both P＜0.05).Conclusion For COPD patients using multi-slice spiral CT scan,low-dose scanning can not only meet the requirements of clinical diagnosis,but also significantly reduce the patient radiation dose.
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Aim To investigate whether pioglitazone has protective effect against glutamate induced neurotoxicity in cultured cortical neurons and its possible molecular mechanisms underlying pioglitazone's neuroprotective effects.Methods The cortical neurons were taken from newborn rats and used for experiments 7 days after culture.The neurons were randomly divided into control group;glutamate group; glutamate+piogli-tazone group;glutamate+SP600125 group;SP600125 group.Cell viability was determined by MTT.The morphology change of neurons was observed under a fluorescence microscope with fluorescence dye Hoechst 33258.Immunostaining was used to investigate the expression of phospho-ATF2 in neuronal cells.Western blot was performed to investigate the protein level of phospho-JNK1 and total JNK1.Results Pioglitazone markedly reduced the damage of cortical neurons caused by glutamate.Pioglitazone also significantly inhibited glutamate induced up-regulation of phospho-JNK1 protein level and phospho-ATF2 expression.SP600125, an inhibitor of JNK, antagonized the toxicity induced by glutamate.Conclusions Pioglitazone can protect cultured cortical neurons from glutamate induced damage.The protective effect of pioglitazone appears to be associated with inhibiting the c-Jun N-terminal protein kinase signaling pathway.
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AIM To observe the neuroprotective effect and protective mechanisms of ibuprofen on amyloid β-protein fragment 1-40 (Aβ1-40)-induced neurotoxicity in rat hippocampus.METHODS Rats were given ibuprofen (15 mg·kg-1 daily,ig) for 3 weeks prior to icv single dose of Aβ1-40 (5 μL,1 mmol·L-1).Six hours after Aβ1-40 injection,Western blotting was used to determine the expressions of phospho-MAP kinase kinase (MKK)3/MKK6,phospho-p38 MAP kinase,phospho-MAP kinase activating protein kinase 2 (MAPKAPK2),heat-shock protein 27(Hsp27),procaspase 9,3,and 7 cleavage,and poly (ADP-ribose) polymerase (PARP) cleavage in hippocampal CA1 region.RESULTS Intracerebroventricular injection of Aβ1-40 induced an increase in phosphorylated MKK3/MKK6 and p38 MAP kinase expressions in hippocampal CA1.These increases,in combination with reduced phospho-MAPKAPK2 and phospho-Hsp27 expressions,mediated Aβ1-40-induced the activation of caspases cascades.Ibuprofen (15 mg·kg-1·d-1,3 weeks) significantly prevented Aβ1-40-induced increases in phosphorylated MKK3/MKK6 and p38 MAP kinase expressions.In addition,Aβ1-40-induced decreases in phosphorylated MAPKAPK2 and Hsp27 expressions were abrogated by ibuprofen.Aβ1-40-induced changes in activation of caspases cascades were inhibited by ibuprofen.CONCLUSIONIbuprofen prevents Aβ1-40-induced neurotoxicity through suppression of phosphorylated MKK3/MKK6 and p38 MAP kinase expressions and the up-regulation of phospho-Hsp27 expression.
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AIM To investigate whether Aβ deposit in Alzheimer disease(AD) impairs signal transduction pathway responsible for neuronal survival.METHODSThe rats were randomly divided into six groups:control group and Aβ25-35 group,Aβ25-35+ibuprofen groups (7.5 and 15 mg·kg-1,respectively),Aβ25-35+ibuprofen+LY294002 group,and Aβ25-35+LY294002 group.Rats were given ibuprofen (7.5 and 15 mg·kg-1 daily,ig) for 3 weeks prior to and 1 week after icv single dose of Aβ25-35 (10 μL,1 mmol·L-1).LY294002 was injected icv 1 h before the injection of Aβ25-35.Seven days after Aβ25-35 injection,the hippocampal expressions of P53,Bax,Fas ligand (FasL),Bcl-2 proteins,phospho-Akt/PKB,and phosphorylated 70 ku ribosomal protein S6 kinase (p70S6K) and caspase 3 were determined in the brain tissue preparations from CA1 area with Western blot.The activity of caspase 3 was measured using a caspase 3 colorimetric activity assay kit.RT-PCR was used to show the change of p70s6k mRNA level.RESULTS Aβ25-35 icv injection significantly down-regulated phosphorylated Akt/PKB from 1.32±0.14 to 0.69±0.08 and p70S6K from 0.769±0.028 to 0.479±0.032 in hippocampal CA1 region.These changes were accompanied by increased expressions of the proapoptotic proteins P53,Bax,and FasL and decreased expression of the anti-apoptotic protein Bcl-2 in rat hippocampus.In addition,caspase 3 activity was significantly enhanced in hippocampal CA1 region in Aβ25-35-treated rats compared with control rats.Ibuprofen can reverse these Aβ25-35-induced changes.CONCLUSION Down-regulated anti-apoptotic PI3K/Akt/p70S6K signaling pathway induced by Aβ25-35 in rat hippocampus may contribute to the neuronal damage in AD.Ibuprofen prevents Aβ25-35-induced down-regulation of PI3K/Akt/p70S6K signaling pathway.
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AIM To investigate the neuroprotective effects and possible mechanisms of saponins from Anemarrhena asphodeloides Bge. (SAaB) on neuronal damage induced by amyloid β-protein fragments 25-35 (Aβ25-35). METHODS Cultured mouse peritoneal macrophages were stimulated with Aβ25-35 (20 μmol·L-1) for 0.5, 1, 2 and 6 h or preincubated with SAaB (10, 30 and 100 μmol·L-1)for 10 min or mitogen-activated protein kinase (MAPK) specific inhibitors (p38 MAPK inhibitor SB 203580 and MEK specific inhibitor PD98059) for 30 min prior to the addition of Aβ25-35(20 μmol·L-1). After stimulation with Aβ25-35 for the indicated times, total cellular extracts were prepared for Western blotting of extracellular signal-regulated kinase (ERK) and p38 MAPK. After stimulation with Aβ25-35 for 48 h, the supernatants of cultured macrophages were collected for quantification of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) and protein expression of inducible nitric oxide synthase (iNOS) in macrophages was determined by immunocytochemical staining. To determine whether SAaB has protective effect against neuronal apoptosis mediated by Aβ25-35-induced macrophages activation, macrophages were stimulated with Aβ25-35 in the presence or absence of SAaB (10, 30 and 100 μmol·L-1) for 48 h and then the cell-free supernatant of Aβ25-35-stimulated macrophages was transferred to the culture of cerebellar granule neurons for 72 h. Neuronal apoptosis was quantitated by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. RESULTS Aβ25-35(20 μmol·L-1) significantly induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein expression without affecting total protein levels and in the production of TNF-α and NO in cultured macrophages. Aβ25-35-induced increase of TNF-α production in macrophages involved activation of ERK1/2 signal pathway. Importantly, TNF-α and NO generated by cultured macrophages after Aβ25-35 stimulation may be responsible for the majority of the neuronal apoptosis. SAaB (30 and 100 μmol·L-1) significantly suppressed Aβ25-35-induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein. In addition, SAaB (10, 30 and 100 μmol·L-1) also decreased the level of TNF-α and NO in supernatants of cultured macrophage and inhibited Aβ25-35-induced increase in iNOS protein expression of macrophages. Neuronal apoptosis mediated by Aβ25-35-induced macrophage activation was also significantly attenuated by treatment with SAaB (10, 30 and 100 μmol·L-1). CONCLUSION SAaB protects neurons against the neuronal cell death induced by Aβ25-35. The beneficial effects of SAaB may be related to the reduction of TNF-α and NO from activated macrophage induced by Aβ25-35.
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BACKGROUND: Oxygen-derived free radicals are produced during non-enzymatic glycosylation of diabetic protein and accompanied with decrease in nitrogen monoxide (NO) synthesis so as to cause the calcium increase in cell,evacuation of pykno-granule and apoptosis induced by activating endoenzyme.OBJECTIVE: To observe the effects of non-enzymatic glycosylation inhibitor-aminoguanidine on apoptosis of cardiac myocyte and cardiac function in diabetic rats.DESIGN: Completely randomized grouping design and controlled study.SETTING: Pharmacological Department of Jinzhou Medical College.MATERIALS: The experiment was completed at the Central Laboratory of Jinzhou Medical College between September 2002 and March 2003. Totally 54 male SD rats with 2-month old were selected.METHODS: Totally 36 rats were selected to establish diabetic model 60 mg/kg of streptozotocin were injected into the caudal vein. If blood glucose of rats was more than 16.7 mmol/L, the establishment of diabetic model was successful. Model rats were divided into diabetes group and aminoguanidine (AG) group with 18 in each group. Rats in each group were also divided into two 12-week groups with 8 and 12 respectively. Another 18 rats were determined as the control group at 2 time points: 12 weeks (n=8) and 24 weeks (n=10). Rats in each group were fed for 12 and 24in other two groups. Calculation of mass index was [heart (mg)/body mass (g)]. Myocardial tissue of left ventricle was taken out and observed with transmission electron microscope and then stained with in situ end-labeling (ISEL) method. Number of positive nucleus was counted with 10 × 10 ocular lens check system and with 10 fields ISEL method; meanwhile, their average was obtained.MAIN OUTCOME MEASURES: Whether there was apoptosis of cardiac cell and the effect on AG in changes of cardiac structure and function of diabetic rats or not.RESULTS: Eight rats were lost during the experiment because of death mass: That of rats in the 12-week and 24-week diabetic group was higher decrease and increase rate of pressure in left ventricle: That of rats in the 12-week and 24-week diabetic group was lower than that in the control in left ventricle: That in 24-week diabetes group was obviously lower than diabetic group was obviously more than that in AG group (P ＜ 0.01), and that in 24-week diabetes group was obviously more than that in 12-week Apoptosis could be observed in myocardial cell in diabetic group.CONCLUSION: Apoptosis of myocardial cell plays an important role in the development of heart failure in diabetic rats. AG can reduce the apoptosis of myocardial cell and decrease the myocardial pathomorphological abnormality.
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AIM: To study the effect of puerarin (Pue) on related cytokines in myocardial hypertrophy induced by isoproterenol (Iso) in rats. METHODS: 40 SD rats were randomly divided into 4 treatments groups: control group, Iso group, Iso+Pue group (Pue group) and Iso+Captoril (Cap) group (Cap group), with 10 rats each group. Ratio of ventricle weight to heart weight, cardiomyocyte diameter, plasma and myocardial tissue NO, ET and Ang Ⅱ levels were measured. RESULTS: Compared with the control group, Iso did induce significant changes in cardiac hypertrophy (P
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AIM For the evaluation of algorithms for circulator drug delivery, a new simulator was developed. METHODS The Clement Yu's non-linear canine circulatory system model was modified for the use of the part of digital dog of the simulator. And the other parts of the simulator were built by the means of object-oriented designing (OOD) with Visual C++ language. The proportion of mean arterial blood pressure in the range of?0.667 kPa of the object value was contracted to T_ MAP , and the average value of integral of excess of the range above was contract to S_ MAP . The difference of T_ MAP and S_ MAP of SPN MMAC(Multiple Model Adaptive Control) controlled hypotension and SPN constant-rate-controlled hypotension had been studied in vivo. This process was repeated in simulation system. The difference of simulator and animal experiments was studied while they were evaluating the SNP MMAC algorithms for controlled hypotension. RESULTS The mean arterial blood pressure graphs of the simulator and animal experiments acted similarly when they evaluated the SNP MMAC algorithms. The graph of mean arterial blood pressure of simulation was similar to that of the animal experiment when the MMAC was evaluated. CONCLUSION The new simulator can evaluate algorithms for circulator drug delivery and it's helpful to the building of such systems.-
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Objective To investigate the effect of pyrrolidine dithiocarbamate(PDTC)on Pseudomonas aeruginosa induced pneumoneia of rats.Metheds A PA induced pneumonia model was established in Sprague-Dawley(SD)rats.Sixty minutes before PA exposure,PDTC and normal saline were injected into abdominal cavity separately.At 3,9,and 24 h after PA exposure,the rats were sacrificed,and the wet/dry ratio(W/D)of lung tissue was measured and histopathologic changes were observed.The number of in-filtrated polymorphonuclear(PMN)leukocytes was calculated.Immunohistochemical staining with activated NF-?B antibody was performed to detect the expression of NF-?B in lung tissues.The changes of IL-8 levels in bronchoalveolar lavage were identified by ELISA.Results Histology findings demonstrated that PA exposure induced obvious changes in lung structure,and edema and pronounced inflammatory cells infiltration were observed.Both symptoms and lesions of lung were lesser in the rats of PDTC group than those of the PA group.Compared with PDTC group,the activation of NF-?B and the expression of IL-8 were significantly up-regulated after PA challenge 3~24 h(P
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Aim To study the effects of sodium ferulate on A?induced cognitive deficits and expressions of IL-1? and phospho-p38MAPK proteins.Methods Alzheimers disease model of rats was produced by intracerebroventricular injection of A?_(25-35)(10 ?g,once).Morris water maze was used to measure spatial memory performance.Nissl staining and immunohistochemical technique for glial fibrillary acidic protein(GFAP) were employed to determine the morphology of pyramidal neurons and astrocyte infiltration in hippocmpal CA1 regions.The levels of phospho-p38MAPK and IL-1? were determined by Western blot and ELISA method.Reverse transcription-PCR analysis showed changes in FasL mRNA.Results Intracerebroventricular injection of A?_(25-35)in rats resulted in spatial memory impairments shown by longer escape latency and decreased percentage of time spent in the target quadrant.These behavioral dysfunctions were accompanied by astrocyte activation and infiltration,increased IL-1? production and elevated FasL mRNA level,the loss of pyramidal neurons in hippocampal CA1,and the increase of phosphorylated p38MAPK.Oral administration of sodium ferulate(50,100,250 mg?kg~(-1)daily) and ibuprofen 15 mg?kg~(-1)daily markedly improved the memory impairment,attenuated pyramidal neuronal damage,and reversed the A?-induced increases in IL-1? and p38MAPK activation.Conclusion sodium ferulate prevents A?-induced neurotoxicity through suppressions of inflammatory response and the activation of p38MAPK.
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AIM To study the antiperoxide damage of injectio tanshin during dissolving thrombus to cure the acute myocardial infarction(AMI). METHODS AMI model formatted by electricity to irritate the left ventricular branch of coronary artery of open-chest rabbit,and observation aspects including electrocardiogram(ECG),cardiac output and contractility,serumal enzymatic activities and biochemistry and pathology of lipid peroxide extent of myocardial infarction zone. RESULTS By urinate kinase(UK) combining with injection tanshin,abnormal changes of ECG, descending of cardiac contractiles and cardiac output,going up of serum cardiac damage enzyme(CPK-MB and LDH),and the malondialdehyde(MDA)of serum and myocardial infarction zone could be remarkably reduced or avoided during UK dissolving the thrombus to cure AMI rabbits. CONCLUSION Injection tanshin can clearly reduce or avoid lipid peroxidation damage during UK dissolving the thrombus to cure the acute myocardial infarction.
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Objective To evaluate the effect of ischemic preconditioning(IPC) on ischemia-reperfusion-injury of myocardium and phosphorylated Akt(p-Akt) during the disease course of diabetes in rats.Methods The rat model of diabetes mellitus was reprodused by streptozocin(40mg/kg,i.v.).Myocardial ischemia was then created by temporary ligation of a branch of the left anterior descending(LAD) coronary artery after 2 and 9 weeks,respectively.Thirty six SD rats were randomly divided into six groups(6 each):non-diabetic IPC(NDMIP) group,non-diabetic I/R(NDMIR) group,2-week diabetic IPC(2DMIP) group,2-week diabetic I/R(2DMIR) group,9-week diabetic IPC(9DMIP) group and 9-week diabetic I/R(9DMIR) group.Ischemic/reperfusion was induced by temporary occlusion of LAD coronary artery.After the experiment,creatine kinase-MB(CK-MB) isoenzyme and myocardial infarct size were measured,and the expression of p-Akt was detected by Western-blotting,the arrhythmia score was then evaluated.Results CK-MB level in NDMIP group was significantly lower than that in NDMIR group and 9DMIP group(P0.05);the arrhythmia score in 9DMIP group was significantly higher than that in 2DMIP group(P0.05);the expression of p-Akt in 9DMIP group was significantly lower than that in 2DMIP group(P0.05);the myocardial infarct size in 9DMIP group was larger than that in 2DMIP group.Conclusions IPC can provide significant microvascular protection against prolonged ischemia/reperfusion in acute diabetic rats,but not in chronic diabetic rats.The attenuation of myocardial protection by IPC may be associated with a decrease in p-Akt activation.