低能激光照射对大鼠梗死后心肌组织的影响

Effects of low-level laser irradiation on the tissue of rats after myocardial infarction

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）。LLu组应用低能激光开胸单次照射后，以逆转录一聚合酶链反应（RT-PCR）法和Westernblot法检测LLu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LLu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VEGFmRNA和蛋白的表达（2．12±0．58、1．02±0．41）及Sham组VEGFmRNA和蛋白的表达（2．42±0．26、0．92±0．37）比较，LLu组显著提高了照射区域梗死后心肌组织中VEGFmRNA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LLu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。

Objective To investigate the influence of low-level laser irradiation （LLLI） on myo- cardial infarction. Methods In LLLI preconditioning study, vascular endothelial growth factor （VEGF）, superoxide dismutase （SOD） and malondialdehyde （MDA） in the infarcted myocardium were evaluated at 1st h, 1st day and 1st 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 or- ganization 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 in- creased, 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 im- prove microenvironment after myocardial infarction, promote cell regeneration and repair after myocardial infarction.