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机构地区:[1]第三军医大学西南医院全军烧伤研究所,创伤,烧伤与复合伤国家重点实验室,重庆400038 [2]河北省宁晋县中西医结合医院
出 处:《中华烧伤杂志》2004年第5期271-274,共4页Chinese Journal of Burns
基 金:国家杰出青年科学基金资助项目 ( 3 0 12 5 0 40 ) ;国家重点基础研究发展规划资助项目(G19990 5 42 0 2 );全军"十五"指令性课题资助项目 ( 0 1L0 66);高等学校骨干教师资助计划项目 ;军队首批临床高新技术重大项目 (第 2 3项 )
摘 要:目的 观察严重烧伤后早期大鼠心肌的过氧化损伤对其线粒体DNA(mtDNA)的影响。方法 将 36只SD大鼠随机分为假烫组、30 %TBSAⅢ度烫伤 1、3、6、12、2 4h组 ,半定量PCR法测定大鼠心肌mtDNA缺失情况 ,取各组大鼠心肌组织匀浆后测定超氧化物歧化酶 (SOD)活性及丙二醛(MDA)含量。 结果 假烫组大鼠心肌mtDNA未见缺失 ;伤后 1、3、2 4h组大鼠心肌mtDNA出现4 834bp大片段的部分或完全缺失 (P<0.0 5或 0 .0 1)。与假烫组比较 ,伤后 1h组大鼠心肌组织中SOD活性明显下降 ,而MDA含量明显升高 (P <0.0 5 );伤后 6h组SOD活性达最低值 (76 .90± 8.30 )U/mg、MDA含量达最高值 (3.17± 0 .80 )nmol/mg( P <0.0 1)。 结论 烧伤后早期大鼠心肌组织受到严重的过氧化损伤 。Objective To investigate the influence of peroxidative injury in rat myocardium on the mitochondrial DNA (mtDNA) during early postburn stage. Methods Thirty-six Sprague-Dawley (SD) rats were employed in the study and were randomly divided into sham scald(SS) and scald groups. The rats in scald groups were inflicted with 30%TBSA Ⅲ degree scalding and were further divided into 1, 3, 6 ,12 and 24 post-scald hour (PSH) groups. The mtDNA deletion was determined by semi-quantitative PCR. The rat myocardial tissue samples were harvested and homogenized and the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined. Results There was no mtDNA deletion in the rat myocardium in SS group. Partial or complete large fragment (4.8kb) mtDNA deletion in the rat myocardium was identified at 1, 3 and 24 PSHs (P<0.05 or 0.01). The SOD activity in the rat myocardium significantly decreased at 1 PSH, reaching the lowest level (76.90±8.30 U/mg) at 6 PSH, but the MDA content increased evidently at 1PSH, peaking [(3.17±0.80) nmol/mg] at 6 PSH(P<0.05). Conclusion Peroxidative injury to the rat myocardium during early postburn stage might be the principal cause of the 4834 bp deletion of mtDNA in rat myocardium.
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