己酮可可碱对心肌肥厚大鼠基质金属蛋白酶2和9表达的影响

目的观察基质金属蛋白酶2和9在心肌肥厚大鼠模型中的变化,并采用己酮可可碱进行干预,以确定己酮可可碱对基质金属蛋白酶的影响及其在心肌肥厚过程中的作用。方法24只雄性SD大鼠随机分为对照组、去甲肾上腺素造模组(模型组)和去甲肾上腺素 己酮可可碱组(治疗组)。采用VG染色评价组织胶原表达,并测定心肌组织胶原含量,免疫组织化学法检测心肌组织基质金属蛋白酶2和9的蛋白表达。结果模型组大鼠发生左心室肥厚,胶原含量显著高于对照组(1.929±0.514mg/g比1.009±0.442mg/g,P<0.01);基质金属蛋白酶2和9表达(分别为131.1±9.8、125.3±4.1)显著低于对照组(P<0.01)。己酮可可碱治疗组心肌总胶原含量较模型组显著降低(1.151±0.215mg/g,P<0.01);基质中基质金属蛋白酶2和9的表达(分别为153.5±6.9、149.5±5.3)较模型组显著增高(P<0.01)。结论己酮可可碱能有效防治心肌肥厚的发生及细胞外基质重塑,这一效应可能与其降低心肌组织中基质金属蛋白酶2和9的高表达有关。

The Effects of Pentoxifylline on the Protein Expression of matrix metalloproteinase-2 and 9 in Rat Cardiac Hypertrophy Model

Aim To investigate the changes of matrix metalloproteinase-2 and 9(MMP-2,MMP-9)in rat cardiac hypertrophy,and the effects of Pentoxifylline(PTX)on it in a rat model.Methods Twenty-four male SD rats were randomly divided into control group,norepinephrine(model)group and norepinephrine + PTX(treated)group.The rat cardiac hypertrophy models were established by intraperitoneal injection of norepinephrine(NE)twice a day for 15 days.Extracellular matrix remodeling was evaluated by morphological examination,stained with Van-Gieson(VG).The content of hydroxyproline in the tissue of myocardium was measured.The protein expression of MMP-2 and MMP-9 were examined by immunohistochemical analysis.Results NE-induced hypertrophy and extracellular matrix remodeling predominantly occurred in the left ventricular,the expression of the collagen(1.929±0.514 mg/g vs 1.009±0.442 mg/g,p<0.01)elevated obviously;the average of the grave scale of protein expression of the MMP-2(131.1±9.8)and MMP-9(125.3±4.1)were lower than those of the control group obviously(p<0.01);After PTX treatment,the collagen(1.151±0.215 mg/g)was decreased and the average of the grave scale of protein expression of MMP-2(153.5±6.9)and MMP-9(149.5±5.3)were higher than those of the model group prominently(p<0.01).Conclusion Pentoxifylline can prevent the cardiac hypertrophy and extracellular matrix remodeling,which was associated with the attenuation of myocardial MMP-2 and MMP-9.