丹参酮ⅡA对大鼠肺缺血再灌注损伤细胞凋亡及相关蛋白表达的影响

目的研究丹参酮ⅡA对大鼠肺缺血再灌注损伤过程中细胞凋亡以及相关蛋白表达的干预作用。方法健康SD大鼠60只随机分成四组，除对照组外，均建立肺缺血再灌注模型，其中两组分别加丹参酮ⅡA和生理盐水干预，检测肺组织湿／干重比、细胞凋亡率、Bcl-2及Caspase-3的表达等指标。结果肺缺血再灌注组与对照组相比，肺组织湿／干重比明显增高，流式细胞仪检测出现大量的凋亡细胞，证明该模型制备是成功的；肺缺血再灌注组显示有统计学意义的凋亡，Bcl-2降低和Caspase．3增高与对照组比较有统计学意义；丹参酮组与未干预组和生理盐水组比较，Bcl-2增高和Caspase-3降低均有统计学意义。结论丹参酮能够改善由肺缺血再灌注引起的细胞凋亡，其机制可能与丹参酮能干预肺组织Bcl-2和Caspase-3蛋白的表达有关。

The Effects of Tanshinone IIA on Apoptosis and the Related Proteins During after Lung Ischemia Reperfusion Injury in Rats

Objective To investigate the effects of Tanshinone on apoptosis and the related proteins during lung ischemia reperfusion injury（LIRI） of rats. Methods Sixty rats were randomly divided into four groups. Apoptotic cells in lung tissue was inspected by flow cytometry and Hematoxylin and Eosin staining, and the expression of Bcl-2 and caspase-3 was detected by RT-PCR and western blot. Results Compared with normal control group, apoptotic cells and the expression of Bcl-2 and Caspase-3 in LIRI model group were markedly increased （P 〈 0. 01 ）. Compared with model group,tanshinone could significantly inhibite cell apoptosis and the expression of apoptosis-related proteins in lung tissues（P 〈0.05）. Conclusion Tanshinone can protect lung from ischemia reperfusion injury by modulating the expression of apoptosis-related proteins Bcl-2 and Caspase-3.