CAJ | 학술논문

目的观察抑肽酶对脑出血大鼠脑内损伤区凝血酶敏感蛋白( TSP ) -1和TSP-2及其受体CD36 mRNA的影响,探讨抑肽酶治疗脑出血的机制.方法将SD大鼠随机分为假手术组、模型组、抑肽酶组,采用胶原酶诱导建立大鼠脑出血模型,运用逆转录-聚合酶链反应( RT-PCR )法观察脑出血后TSP-1及TSP-2和CD36 mRNA表达变化.结果脑出血第4天,TSP-1表达达高峰;TSP-2第14天表达达高峰;脑出血第4天,第21天CD36呈双峰表达.抑肽酶组TSP-1 mRNA表达第1~4天明显高于模型组( P<0. 01 );TSP-2 mRNA第14天达高峰且第1~21天均明显高于模型组( P<0. 05 );CD36 mRNA第1~4天表达明显低于模型组( P<0. 05 ) ,第14~21天明显高于模型组( P<0. 01 ).结论抑肽酶可能通过调整脑出血大鼠脑内TSP-1及TSP-2和CD36 mRNA的表达,降低其对血管新生的抑制作用,加快血肿吸收,促进脑组织修复.
목적 관찰억태매대뇌출혈대서뇌내손상구응혈매민감단백( TSP ) -1화TSP-2급기수체CD36 mRNA적영향,탐토억태매치료뇌출혈적궤제.방법 장SD대서수궤분위가수술조、모형조、억태매조,채용효원매유도건립대서뇌출혈모형,운용역전록-취합매련반응( RT-PCR )법관찰뇌출혈후TSP-1급TSP-2화CD36 mRNA표체변화.결과 뇌출혈제4천,TSP-1표체체고봉;TSP-2제14천표체체고봉;뇌출혈제4천,제21천CD36정쌍봉표체.억태매조TSP-1 mRNA표체제1~4천명현고우모형조( P<0. 01 );TSP-2 mRNA제14천체고봉차제1~21천균명현고우모형조( P<0. 05 );CD36 mRNA제1~4천표체명현저우모형조( P<0. 05 ) ,제14~21천명현고우모형조( P<0. 01 ).결론 억태매가능통과조정뇌출혈대서뇌내TSP-1급TSP-2화CD36 mRNA적표체,강저기대혈관신생적억제작용,가쾌혈종흡수,촉진뇌조직수복.
Objective To observe the influence of aprotinin on the expressions of thrombospondin ( TSP ) -1, TSP-2 and their receptor CD36 in rats' brains of intracerebral hemorrhage ( ICH ) and to explore its mechanisms. Methods SD rats were randomly divided into 3 groups:sham operated group, ICH model group, and aprotinin therapy group. The rat model of cerebral hemorrhage was induced by colla-genase; the distribution of TSP-1, TSP-2 and CD36 were assayed by reverse transcription polymerase chain reaction ( RT-PCR ) . Results TSP-1 arrived at the peak on the 4th day after ICH ( P < 0. 01 );TSP-2 arrived at the peak on the 14th day while CD36 on the 4th day and 21st day. In Aprotinin therapy group, the expression of TSP-1mRNA was notably higher than that of ICH model group from the 1st day to 4th day ( P < 0. 01 );TSP-2 mRNA arrived at the peak on the 14th day and was higher than that of ICH model group from the 1st day to 21st day of ICH ( P < 0. 05 ) . CD36 was lower from the 1st day to 4th day of ICH ( P < 0. 01 ) but higher from the 14th day to 21sth day of ICH( P < 0. 01). Conclusion Aprotinin could regulate the expressions of TSP-1, TSP-2 and CD3636mRNA in rats after ICH to lower the depressant effects on angiogenesis, accelerate the absorption of hematomas and promote cerebral tissue repair.