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The Effect Of PTX3 On Atrial Myocytes IL-6,TNF-α,NF-κB P65 In Patients With Chronic Atrial Fibrillation

Posted on:2012-08-29Degree:MasterType:Thesis
Country:ChinaCandidate:Z Y NiFull Text:PDF
GTID:2154330335951010Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
AF is one of the most common clinical cardiac arrhythmia. Its prevalence rate of people over 30 years old is 0.77% in China, and the rate increases with age. It is a serious harm to human health. The highly complications,disability and death rate,poor efficacy of AF make people take increasing emphasis on its mechanism. In recent years, it is found that AF is an inflammatory reaction. IL-6,TNF-α,signal transduction pathway of NF-κB are important parts of inflammation. But the conclusions of related reports are inconsistent. PTX3 is a new factor of inflammatory found recently. But the effect of PTX3 on AF has not been recognized clearly and there is little report about the relationship between PTX3 and IL-6,TNF-α,signal transduction pathway of NF-κB. This study analyzed the effect of PTX3 on AF through the change of the level of IL-6,TNF-a and the gene expression of NF-κB P65 stimulated by PTX3. Our purpose is to evaluate the condition of AF in clinic and to provide a theoretical basis on inflammation associated with AF.Purpose:To discuss the effect of PTX3 in atrial muscle cells of patients with chronic atrial fibrillation and to provide a theoretical basis on inflammation associated with AF.Methods:1.Research object:According to Declaration of Helsinki,22 patients suffering cardiac surgical operation are selected after gaining preoperational discussion of Ethics Committee and permission of patients and family members,11 in AF group,6 men and 5 women with age of 41.5±4.3 years,9 patients have II degree heart function,2 patients haveⅢdegree heart function, no additional arrhythmia medical history,AF time is over 1 year,11 in SR group,5 men and 6 women with age of 40.7±5.3 years.8 patients have II degree heart function,3 patients haveⅢdegree heart function, no arrhythmia medical history. Age, gender, heart function NYHA grade, electrocardiogram, ultrasonic cardiogram and related laboratory examination are all recorded in the two groups. Hyperthyroidism, dilated cardiomyopathy. chronic pulmonary heart disease, acute infection, fat, rheumatic disease, blood and hemopoietic system disease, internal secretion and metabolic disease, serious liver dysfunction, recent application of antibiotics, aspirin (exclusive of disuse 7 days before operation), ACEI and ARB, statins adjustment lipid deugs are all not listed in this research scope.2. Sample collection:Extracorporeal circulation should be established in the cardiac surgery and 100mg auricula dextra before cardiac arrest should be acquired, removing blood and adipose tissue. Put it in 10ml oxygen-saturation non-calcium liquor under 37℃preservation and send it to the laboratory within 5-10 minutes. The AF component is made into two parts. One is joined PTX3 with 1ml which concentration is 12μg/mL. The other one and the SR group are put in the thermostat together, affected for one hour, and the supernate is collected.3. Analysis methods:The level of NF-κB P65 gene expression in atrial cadiocyte was determined by reverse transcription polymerase chain reaction(RT-PCR) and Western Blot. The levels of IL-6 and TNF-a were determined by enzyme linked immunosorbent assay(ELISA). All the data was analyzed by the statistical processing of SPSS 13.0.Results:(1)The level of NF-κB P65 gene expression in atrial cadiocyte of patients in the group with AF was higher than that in the group with SR. The level of NF-κB P65 gene expression in atrial cadiocyte of patients in the group with AF stimulated by PTX3 was higher than that in the group with AF. The difference was statistically significant.(2) The levels of IL-6 and TNF-a in atrial cadiocyte of patients in the group with AF were higher than that in the group with SR. The levels of IL-6 and TNF-αin the group with AF stimulated by PTX3 were higher than that in the group with AF. The difference was statistically significant.Conclusion:(1) IL-6,TNF-αand NF-κB take part in pathological process of AF.(2)PTX3 promotes inflammation reaction of AF and makes it worse through the effect on IL-6,TNF-α,and NF-κB.(3) It is speculated that inflammation reaction is one of the cause which leads to the occurrence and maintain of AF.
Keywords/Search Tags:AF, PTX3, IL-6, TNF-α, NF-κB
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