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目的 探讨基质金属蛋白酶３（ＭＭＰ－３）ｍＲＮＡ转录在肺动脉高压肺血管重建中的可能作用。方法 利用野百合碱（ＭＣＴ）诱导的大鼠肺动脉高压动物模型，经右心导管介入测定大鼠肺动脉平均压，ＲＴ－ＰＣＲ法检测不同时间点大鼠肺组织ＭＭＰ－３ｍＲＮＡ表达水平以及比色法测定主肺动脉段羟脯氨酸含量。结果 实验第２１ｄ肺动脉压力已明显升高，以第２８ｄ为最高，而大鼠肺组织ＭＭＰ－３ｍＲＮＡ表达水平以第７ｄ最高，第１４、２１、２８ｄ依次逐渐下调，第２１ｄ已接近正常组水平，而主肺动脉段羟脯氨酸含量第１４ｄ异常降低，以后随肺动脉压力的升高而升高。结论 ＭＭＰ－３早期转录水平升高可能与肺血管基底膜降解有关，参与对肺血管重建的触发作用，实验后期转录水平下调可能是导致细胞外基质积聚的重要原因之一。
Objective To investigate the possible role of matrix metalloproteinase 3 (MMP-3) mRNA transcription in pulmonary vascular remodeling in pulmonary hypertension. Methods The rat model of pulmonary hypertension induced by monocrotaline (MCT) was established. The mean pulmonary arterial pressure was measured by right heart catheterization. The expression of MMP-3 mRNA in lung tissue of rats at different time points was detected by RT-PCR. Determination of the main pulmonary artery hydroxyproline content. Results The pulmonary artery pressure was significantly increased on the 21st day and reached its peak on the 28th day. The expression of MMP-3 mRNA in the lung tissue of rats was highest on the 7th day, and gradually decreased on the 14th, 21st and 28th day, and close to the normal level on the 21th day. The main pulmonary artery hydroxyproline content 14d anomaly decreased, with the increase of pulmonary artery pressure and then increased. Conclusions The increased expression of MMP-3 in early stage may be related to the degradation of pulmonary vascular basement membrane, which may be involved in the triggering of pulmonary vascular remodeling. Down-regulation of transcription may be one of the important reasons leading to extracellular matrix accumulation.