摘要
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 m RNA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 m RNA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 m RNA表达第1~4天明显高于模型组(P<0.01);TSP-2m RNA第14天达高峰且第1~21天均明显高于模型组(P<0.05);CD36 m RNA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 m RNA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。
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.
出处
《中国药业》
CAS
2015年第21期22-24,共3页
China Pharmaceuticals
基金
四川省南充市重点科技资助项目
项目编号:N2008-SF010