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Objective:To analyze the influences of azithromycinantibiotic combined glucocorticoids on the levels of erythrocyte sedimentation rate (ESR),serum lactate dehydrogenase (LDH) and inflammatory cytokines levels as well as the clinical effect of severe pneumonia mycoplasma.Methods:112 children with severe pneumonia mycoplasma who were treated in our hospital were selected and randomly divided into the control group and the observation group with 56 cases in each group.The patients in the control group were treated with azithromycinantibiotic,while the patients in the observation group were treated with glucocorticoid on the basis of the control group.Then the levels of ESR,LDH,isoenzyme MB (CK-MB),creatine kinase (CK),aspertate aminotransferase (AST),c-reactive protein (CRP),interleukin 6 (IL-6),tumor necrosis factor-o (TNF-α),CD4+ and CD8+,the clinical efficacy and adverse reactions between two groups were observed and compared before and after the treatment.Results:The effective rate in the observation group was higher than that of the control group,and the difference was statistically significant (P＜0.05).After treatment,the levels of ESR,LDH,CK-MB,CK,AST,CRP,IL-6,TNF-α and CD8+ in the two groups decreased,which were lower in the observation group than those of the control group (P＜0.05).After treatment,the levels of CD4+ in both groups increased,which was higher in the observation group than that of the control group (P＜0.05).The disappearance time of fever,cough relief,lung rale of observation group were shorter than those of the control group(P＜0.05).There was no statistically significant difference in the adverse reactions between the two groups (P＞0.05).Conclusion:Azithromycin combined with glucocorticoids was more effective than azithromycin alone in the treatment of severe mycoplasma pneumonia with high safety,which could obviously relieve the myocardial injury and inflammatory response,enhance the immune function.
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Inflammasomes are molecular platforms built around several proteins ,composed of intracellular pattern-recognition receptors,the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC)and caspase-1. The inflammasome was believed as the cellular machinery triggering the maturation of proinflammatory cytokines such as interleukin-1β(IL-1β)to engage innate immune defenses. Several types of inflammasomes have been identified ,and among them NLRP3 inflam?masome is currently the most fully characterized inflammasome. Recent studies showed that a variety of cardiovascular risk factors , including dyslipidemia,hypertension and kidney disease,hyperhomocysteinemia,obesity,diabetes and metabolic syndrome,can activate NLRP3 inflammasomes,process the maturation of proinflammatory cytokines IL-1βand IL-18,and promote atherosclerosis. The activation of NLRP3 inflammasomes was also associated with decreased stability of atherosclerotic plaque. These studies suggested an important role of NLRP3 inflammasomes in the pathogenesis of cardiovascular disease. Targeting NLRP3 inflammasome at the stage of its assembling or activation may be a novel strategy for prevention and treatment of cardiovascular disease.
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AIM:NLRP3 inflammasome was identified as the cellular machinery responsible for activation of inflammatory processes .The present study investigated whether the activation of NLRP 3 inflammasomes contributes to hyperhomocysteinemia ( HHcy)-induced in-flammation and atherosclerosis .METHODS:ApoE-/-mice were fed regular diet , high fat ( HF) diet or HF plus high methionine (HM) diet for 10 weeks.NLRP3 shRNA or scramble shRNA viral suspension was injected twice at the 2nd and the 6th weeks after HFHM treatment.The whole aortas and aortic root sections were stained with Oil Red O for atherosclerotic lesion .Plasma lipids, ho-mocysteine ( Hcy) , IL-1βand IL-18 levels were measured .We also examined the effect of Hcy on NLRP 3 inflammasomes activation in THP-1 differentiated macrophages in the presence or absence of NLRP 3 siRNA, caspase-1 inhibitor Z-WEHD-FMK, or antioxidant N-acetyl-L-cysteine ( NAC) .RESULTS:HFHM treatment induced HHcy in ApoE-/-mice.Increased plasma levels of IL-1βand IL-18, aggravated macrophage infiltration into atherosclerotic lesion , and accelerated development of atherosclerosis were detected in HHcy mice, which were associated with the activation of NLRP 3 inflammasomes.Silencing the NLRP3 gene significantly suppressed NLRP3 inflammasomes activation , reduced plasma levels of proinflammatory cytokines , attenuated macrophage infiltration , and improved HHcy-induced atherosclerosis .Moreover, we found that Hcy activated NLRP3 inflammasomes and promoted subsequent production of IL-1βand IL-18 in macrophages, which were blocked by NLRP3 gene silencing, Z-WEHD-FMK, or NAC.CONCLUSION:These data suggest that the activation of NLRP 3 inflammasomes contributes to HHcy-induced inflammation and atherosclerosis .Hcy activates NLRP3 inflammasomes in reactive oxygen species dependent pathway in macrophages .
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Functional experiment plays an important role in understanding the mechanisms of diseases and principles of diagnosis and treatment. It requires students to master basic skills of func-tional operation, and complicated disciplines of functional alteration as well. Thus functional experi-ment needs to be an open course. The use of the virtual reality (VR) and real-time recording tech-niques provides potential for this exploration. By the way of real-time recording system, HD video of experiment operation is played, which helps guiding students to learn basic experiment skills; while based on the development status of VR technology, it is more applicable for learning by oneself, such as preview before the class and review for the test, and furthermore, the advantage of VR technique will be more apparent, if the key development focuses on experiment extensions to disclose more compli-cated functional alterations. This new technique helps to improve teaching effects of functional experi-ment.
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Photoreactive heparin was synthesized by reaction of 4-azidoaniline and heparin. An organic layer was introduced on the surface of Ti-O by 3-aminopropylphosphonic acid assembling, and then the modified heparin was immobilized on the surface by UV irradiation. Water contact angle was used to characterize the hydrophilicity, quantitive assay was done by azure staining methods, and blood compatibility was evaluated by platelet adhesion experiment. Water contact angle of heparinized surface was smaller than that of Ti-O film, which indicated more hydrophilic property of heparinized surface. The surface density of heparin increased with the prolonging of irradiation time and the density was 2.1 microg/cm2 when irradiated for 300s. It showed the heparinized surface was effective in resisting platelets from adhesion and aggregation.
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Humans , Aniline Compounds , Chemistry , Azo Compounds , Chemistry , Blood Proteins , Pharmacology , Fibrinolytic Agents , Pharmacology , Heparin , Chemistry , Membranes, Artificial , Propylamines , Chemistry , Surface Properties , Titanium , ChemistryABSTRACT
Objective To investigate the effects of different growth factors to perfused kidney in vitro at room temperature. Methods 25 New Zealand rabbits were randomly divided into 5 groups, Each group had 5 rabbits. Perfusion was carried out in vitro on rabbits′ kidney with different culture media containing hepatocellular growth factor(HGF) in high or low dosage, epidermal growth factor(EGF) in high or low dosage, and growth factors-free. On the 65th hour after perfusion, lactate dehydrogenase(LDH) activity, the concentration of sodium and potassium in kidney vein effluent and ?-N-acetyl amino glucosaminidase in urine (NAG) activity in each group were respectively detected to observe the renal function. Renal histological changes under light microscope and proliferating cell nuclear antigen (PCNA) of renal tissue were also examined to observe the renal morphological changes and the lesion degrees of renal tissue. Results The preservation effect of the culture media containing HGF in high dosage was the best among all 5 groups. In this group, LDH activity, the concentration of potassium in kidney vein effluent and NAG activity in urine were significantly lower than that of other 4 groups; the concentration of sodium of kidney vein effluent was notably higher than any other group. Renal histological changes under light microscope and PCNA stain of renal tissue showed that the renal morphological damage and the lesion of renal tissue were lighter than any other group. Conclusion HGF in high dosage could markedly improve the effect of perfusion preservation and protect the function and morphology structure of perfused rabbits′ kidneys better.
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Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.
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AIM:To establish a microthrombus model by carrageenan (Ca)/ lipopolysaccharides (LPS) intraperitoneal injection in rats with hyperhomocysteinemia (HHcy) and endothelial dysfunction induced by L-methionine intake. METHODS: ① Male Sprague Dawley rats were randomly divided into 2 groups: control and endothelial dysfunction (HHcy) groups. L-methionine was administered by gavage in HHcy group for total 4 weeks. Purified water was administered by gavage in control rats. Plasma Hcy, NO and vWF were examined and the thoracic aorta were excised after 4 weeks of L-methionine treatment to evaluate endothelial function. ② Male Sprague Dawley rats were randomly divided into 3 groups to establish a microthrombus formation model with Ca/ LPS: control, microthrombus formation (Ca/LPS) and endothelial dysfunction plus mitoarothrombus formation (HHcy+Ca/LPS) groups. Control rats were injected with normal saline (NS). Ca/LPS rats were intraperitoneally injected with carrageenan (Ca) and followed by lipopolysaccharides (LPS) 16 h later. HHcy+Ca/LPS rats were intragastric gavaged by L-methionine for total 4 weeks, and then were injected with Ca/LPS in the same way as Ca/LPS group. Cruor parameters and platelet count were detected at 20 h after LPS or NS injection and the mesentery microcirculation was monitored. Plasma NO and vWF were also detected at 24 h after LPS or NS injection. RESULTS: ① Plasma Hcy concentrations and vWF level were significantly increased in HHcy group, while plasma NO content was significantly decreased compared with that in control group. Endothelial dependent relaxation (EDR) of aortic rings was significantly decreased in HHcy group, suggesting endothelial damage/dysfunction was induced by HHcy. ② Mesentery capillary was obviously blocked by microthrombus in Ca/LPS rats and was blocked more seriously in HHcy+Ca/LPS rats. Cruor parameter results suggested that Ca/LPS rats were in hypercoagulable phase and HHcy+Ca/LPS rats were in hypocoagulable phase at 20 h after LPS injection. Platelet count and plasma NO content in HHcy+Ca/LPS group were significantly decreased, while plasma vWF level was significantly increased compared with Ca/LPS group. CONCLUSION: L-methionine intake induces severe HHcy and causes endothelial dysfunction in rats. Microcirculation dysfunction and microthrombosis can be caused by Ca/LPS intraperitoneal injection and may be aggravated by endothelial dysfunction.
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Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.
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AIM: To observe the effects of Sini decoction on atherosclerosis(AS) and ceramide content of aorta in rabbits. METHODS: 28 rabbits were randomly divided into three groups. Control group was fed with a normal diet; High cholesterol group was fed 1% cholesterol and 5% fat diet; Sini decotion+ high cholesterol group was fed 1% cholesterol and 5% fat diet plus Sini decotion (4.2 g?kg -1 ?d -1 ). At the end of study, the plaque area were measured, the atorta ceramide and cell apoptosis were also detected. RESULTS: Sini decotion diminished lipid plaque area on the aortic endothelium, reduced the levels of aorta ceramide and the apoptosis index. CONCLUSION: Sini decoction has an inhibitory effect on AS, the mechanism may be that Sini decotion reduces concentration of ceramide in aorta.
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AIM: To screen the differentially expressed genes among normal, ischemic and Sini decoction-treated myocardium using DNA microarray.METHODS: Kunming mice were randomly divided into control group, ischemic group and Sini decoction group. Total RNA was extracted from myocardium of each group. cDNA microarray chips containing 2 304 cDNAs were used to investigate the gene expression pattern of each group. RESULTS: Up-and down-regulated genes were 33 and 70 in ischemic group vs control group, respectively. Up-and down-regulated genes were 23 and 52 respectively in Sini decoction group vs ischemic group. CONCLUSIONS: The analysis of gene expression pattern of ischemic myocardium based on cDNA microarray can realize high-throughput screening of the genes. Further analysis of those obtained genes information will be helpful to understand the molecular mechanism of myocardial ischemia and the therapeutic mechanism of Sini decoction.
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AIM: To detect the effect of Sini decoction on glutathione S-transferase (GST) mRNA expression in the ischemic myocardium. METHODS: Kunming mice were randomly divided into control group, ischemic group and Sini decoction group. Total RNA was extracted from the myocardium of mice in each group. The effect of Sini decoction on the expression of GST gene was detected by RT-PCR. RESULTS: The expression of GST mRNA in Sini decoction group was significantly up-regulated compared with the ischemic group and control group. CONCLUSION: Sini decoction can promote the expression of GST gene, which may be related to its protective effect on ischemic myocardium.