脑缺血时半乳糖凝集素-3对大鼠脑皮质中bcl-2、BAX及caspase-3表达的影响

Effect of galectin-3 on expression of B-cell lymphoma-2,Bcl-2-asociated X protein,and cysteine aspartic acid-specific protease 3 in rat cerebral cortex during cerebral ischemia

目的通过脑缺血/再灌注损伤模型,测定脑缺血时半乳糖凝集素-3(Gal-3)对B淋巴细胞瘤-2(bcl-2)、Bcl-2相关X蛋白(BAX)及含半胱氨酸的天冬氨酸蛋白水解酶-3(caspase-3)表达的影响,从而为脑缺血的发病机制提供一定的实验依据。方法雄性SD大鼠18只,建立大鼠大脑中动脉阻塞(MCAO)模型,缺血1.5 h,再灌注至24 h。采用随机分组法分为假手术组(sham)、缺血/再灌注组(I/R)和Gal-3 RNA干扰组(siRNA)。采用real-time PCR及western blot检测大鼠脑皮质中Gal-3、bcl-2、BAX及caspase-3 mRNA及蛋白表达变化。结果大鼠脑缺血/再灌注损伤后,脑皮质中Gal-3及bcl-2 mRNA及蛋白表达明显下调,分别为0.38、0.47和1.310、1.299;BAX及caspase-3 mRNA及蛋白表达明显上调,分别为1.41、1.55及1.076、1.155。而Gal-3 RNA干扰后,Gal-3及bcl-2 mRNA及蛋白表达明显下调,分别为0.24、0.14及1.014、1.058;BAX及caspase-3 mRNA及蛋白表达明显上调,分别为1.76、1.88及1.480、1.515。结论 Gal-3可能通过上调bcl-2、下调caspase-3及BAX mRNA及蛋白的表达,参与脑缺血/再灌注损伤的病理过程。

Objective To investigate the effect of galectin-3 （Gal-3） on the expression of B-cell lymphoma-2 （bcl-2）,Bcl-2-associated X protein （BAX）,and cysteine aspartic acid-specific protease 3 （caspase-3） during cerebral ischemia in a model of cerebral ischemia-reperfusion injury,and to provide an experimental basis for the pathogenesis of cerebral ischemia.Methods A total of 18 male Sprague-Dawley rats were given ischemic treatment for 1.5 hours followed by reperfusion to 24 hours to establish a model of middle cerebral artery occlusion,and then these rats were randomly divided into sham-operation group,ischemia-reperfusion （I/R） group,and Gal-3 RNA interference （siRNA） group.Real-time PCR and Western blot were used to measure the changes in the mRNA and protein expression of Gal-3,bcl-2,BAX,and caspase-3 in rat cerebral cortex.Results After cerebral ischemia-reperfusion injury,the I/R group had significant reductions in the mRNA and protein expression of Gal-3 （0.38 and 0.47） and bcl-2 （1.310 and 1.299） and significant increases in the mRNA and protein expression of BAX （1.41 and 1.55） and caspase-3 （1.076 and 1.155）.After Gal-3 RNA interference,the siRNA group had significant reductions in the mRNA and protein expression of Gal-3 （0.24 and 0.14） and bcl2 （1.014 and 1.058） and significant increases in the mRNA and protein expression of BAX （1.76 and 1.88） and caspase-3 （1.480 and 1.515）.Conclusions Gal-3 may participate in the pathological process of cerebral I/R injury by upregulating the mRNA and protein expression of Bcl-2 and downregulating the mRNA and protein expression of caspase-3 and BAX.