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低强度红激光局部照射抑制血管成形术后血管重塑的可能机制 |
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esence of apoptotic VSMC was demonstrated by terminal deoxynucleotidyl transferase-mediated dUTP nickl end labeling (TUNEL) method. Results ①The expression of Col I mRNA at 3rd day after balloon injury, the two groups (LPRLI group vs control group) did not show a significantly difference ［(114±24） cpm vs （118±11）cmp, P＞0.05］. from 1st week to 4th week, the expressions of Col I mRNA showed a significantly difference. The densitometric data of RT-PCR in LPRLI group was lower than the control group ［(760±119） cpm vs （879±121） cpm, P＜0.05；（1 120±300） cpm vs （1 409±297） cpm, P＜0.05; （918±180） cpm vs （1 109±117） cpm, P＜0.05］；②The expression of ICAM-1 from 3rd day to 4th week, the expressions of ICAM-1 in LPRLI group was significantly reduced both at the intima and adventitia ［(0.90±0.48） vs （1.79±0.91）, P＜0.05；（1.41±0.89） vs （3.46±1.57）, P＜0.01; （2.60±0.91） vs （3.51±0.99）, P＜0.05；（2.31±1.00 ）vs （2.57±1.20）, P＜0.05］.③Apoptosis of VSMC. These studies suggested that there were histochemical evidence of apoptosis in all of the injured vessels. There were no quantitative differences in the amount of LPRLI and control vessels at 3 days, 1 week and 8 weeks. But there were marked differences between the two groups. The index of apoptotic VSMC in LPRLI group was higher than control groups (51±19 vs 29±11,P＜0.01;36±12 vs 26±8,P＜0.05). No significantly differences of apoptotic related gene expression were found in the two groups include p53, bcl-2/bax. Conclusion These preliminary findings suggest that LPRLI prevents vascular lesion formation after balloon injury by reducing the expressions of Col I mRNA and ICAM-1. In addition, LPRLI may contribute to induce the apoptosis of VSMC. The results of this study support that LPRLI is a very useful technique in controlling the constrictive vascular remodeling by reduction of vessel constriction and in 上一页 [1] [2] [3] 下一页
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