中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
8期
1568-1570
,共3页
余海彬%法宪恩%高成山%黄真锋%周玉阳%刘雷
餘海彬%法憲恩%高成山%黃真鋒%週玉暘%劉雷
여해빈%법헌은%고성산%황진봉%주옥양%류뢰
低能激光照射%心肌梗死%血管内皮生长因子%超氧化物歧化酶%丙二醛
低能激光照射%心肌梗死%血管內皮生長因子%超氧化物歧化酶%丙二醛
저능격광조사%심기경사%혈관내피생장인자%초양화물기화매%병이철
Low-level laser irradiation%Myocardial infarction%Vascular endothelial growth factor%Superoxide dismutase%Malondialdehyde
目的 观察低能激光照射(LLLI)对大鼠梗死后心肌组织的影响.方法 冠状动脉结扎法制作雌性SD大鼠心肌梗死模型,3周后,经超声筛选合格心肌梗死大鼠随机分为两组:(1)低能激光照射组(LLLI组)；(2)对照组(Control组)；另设假手术组(Sham组).LLLI组应用低能激光开胸单次照射后,以逆转录-聚合酶链反应(RT-PCR)法和Western blot法检测LLLI处理区内心肌组织中血管内皮生长因子(VEGF)的表达,照射后1h、1d、1周,分别测定LLLI处理区内心肌组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.结果 与Control组VEGF mRNA和蛋白的表达(2.12 ±0.58、1.02±0.41)及Sham组VEGF mRNA和蛋白的表达(2.42±0.26、0.92±0.37)比较,LLLI组显著提高了照射区域梗死后心肌组织中VEGF mRNA和蛋白的表达(4.42±2.88、2.62±1.83,P ＜0.05)；Sham组与Control组之间比较差异无统计学意义(P＞0.05).在预处理后1h和1d,与Control组比较,LLLI组梗死后心肌组织中SOD的活性[(0.84±0.43)、(0.92±0.34) U/mg)]均显著提高；而MDA的产量[(0.56±0.31)、(0.50 ±0.29) nmol/mg]显著降低(P＜0.05).在预处理后1周,LLLI组与Control组之间上述指标差异无统计学意义(P＞0.05).结论 LLLI处理显著上调梗死后心肌组织中VEGF的表达及SOD的活性,降低了MDA的含量,从而能够改善梗死后心肌微环境,促进梗死后心肌细胞的再生与修复.
目的 觀察低能激光照射(LLLI)對大鼠梗死後心肌組織的影響.方法 冠狀動脈結扎法製作雌性SD大鼠心肌梗死模型,3週後,經超聲篩選閤格心肌梗死大鼠隨機分為兩組:(1)低能激光照射組(LLLI組)；(2)對照組(Control組)；另設假手術組(Sham組).LLLI組應用低能激光開胸單次照射後,以逆轉錄-聚閤酶鏈反應(RT-PCR)法和Western blot法檢測LLLI處理區內心肌組織中血管內皮生長因子(VEGF)的錶達,照射後1h、1d、1週,分彆測定LLLI處理區內心肌組織中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.結果 與Control組VEGF mRNA和蛋白的錶達(2.12 ±0.58、1.02±0.41)及Sham組VEGF mRNA和蛋白的錶達(2.42±0.26、0.92±0.37)比較,LLLI組顯著提高瞭照射區域梗死後心肌組織中VEGF mRNA和蛋白的錶達(4.42±2.88、2.62±1.83,P ＜0.05)；Sham組與Control組之間比較差異無統計學意義(P＞0.05).在預處理後1h和1d,與Control組比較,LLLI組梗死後心肌組織中SOD的活性[(0.84±0.43)、(0.92±0.34) U/mg)]均顯著提高；而MDA的產量[(0.56±0.31)、(0.50 ±0.29) nmol/mg]顯著降低(P＜0.05).在預處理後1週,LLLI組與Control組之間上述指標差異無統計學意義(P＞0.05).結論 LLLI處理顯著上調梗死後心肌組織中VEGF的錶達及SOD的活性,降低瞭MDA的含量,從而能夠改善梗死後心肌微環境,促進梗死後心肌細胞的再生與脩複.
목적 관찰저능격광조사(LLLI)대대서경사후심기조직적영향.방법 관상동맥결찰법제작자성SD대서심기경사모형,3주후,경초성사선합격심기경사대서수궤분위량조:(1)저능격광조사조(LLLI조)；(2)대조조(Control조)；령설가수술조(Sham조).LLLI조응용저능격광개흉단차조사후,이역전록-취합매련반응(RT-PCR)법화Western blot법검측LLLI처리구내심기조직중혈관내피생장인자(VEGF)적표체,조사후1h、1d、1주,분별측정LLLI처리구내심기조직중초양화물기화매(SOD)활성화병이철(MDA)함량.결과 여Control조VEGF mRNA화단백적표체(2.12 ±0.58、1.02±0.41)급Sham조VEGF mRNA화단백적표체(2.42±0.26、0.92±0.37)비교,LLLI조현저제고료조사구역경사후심기조직중VEGF mRNA화단백적표체(4.42±2.88、2.62±1.83,P ＜0.05)；Sham조여Control조지간비교차이무통계학의의(P＞0.05).재예처리후1h화1d,여Control조비교,LLLI조경사후심기조직중SOD적활성[(0.84±0.43)、(0.92±0.34) U/mg)]균현저제고；이MDA적산량[(0.56±0.31)、(0.50 ±0.29) nmol/mg]현저강저(P＜0.05).재예처리후1주,LLLI조여Control조지간상술지표차이무통계학의의(P＞0.05).결론 LLLI처리현저상조경사후심기조직중VEGF적표체급SOD적활성,강저료MDA적함량,종이능구개선경사후심기미배경,촉진경사후심기세포적재생여수복.
Objective To investigate the influence of low-level laser irradiation (LLLI) on myocardial infarction.Methods In LLLI preconditioning study,vascular endothelial growth factor (VEGF),superoxide dismutase (SOD) and malondialdehyde (MDA) in the infarcted myocardium were evaluated at 1 st h,1 st day and 1 st week after laser irradiation.Results LLLI significantly increased VEGF mRNA and protein expression (4.42 ±2.88 and 2.62 ± 1.83) in the irradiated region after myocardial infarction organization as compared with cntrol group (2.12 ± 0.58 and 1.02 ± 0.41) and sham group (2.42 ± 0.26 and 0.92 ± 0.37,P ＜ 0.05),and there was no significant difference between sham group and control group.After pretreatment for 1 h and 1 day,as compared with control group,the enzymatic activity of SOD in the LLLI infarct myocardial tissue [(0.84 ± 0.43) and (0.92 ± 0.34) U/mg] was significantly increased,and MDA production [(0.56 ±0.31) and (0.50 ± 0.29) nmol/mg] was significantly reduced (P ＜ 0.05).These indicators one week after pretreatment between LLLI group and control group showed no statistically significant difference (P ＞ 0.05).Conclusion LLLI treatment significantly raised VEGF expression and SOD activity in the infarction myocardial tissue,and reduced MDA content,which can improve microenvironment after myocardial infarction,promote cell regeneration and repair after myocardial infarction.
