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目的　探讨ｍｉｃｒｏＲＮＡｓ-４５５（ｍｉＲ-４５５）在心室重构中的作用及其机制。方法　选择小鼠１８只，分为 ｍｉＲ-４５５组、ＧＦＰ组及假手术组各６只。ｍｉＲ-４５５组、ＧＦＰ组均行升主动脉缩窄术，术后４周即进展为心室重构模 型。假手术组术中仅游离主动脉弓但不结扎。ｍｉＲ-４５５组于术后第１、８、１５、２２天尾静脉注射包被ｍｉＲ-４５５的腺病 毒０．１ｍＬ，ＧＦＰ组及假手术组于同时点尾静脉注射包被ＧＦＰ的腺病毒０．１ｍＬ。术后４周造模成功，应用心脏超声 检查测量各组左心室舒张期内径（ＬＶＩＤｄ）、左心室舒张末容积（ＬＶＥＤＶ）、左心室舒张期前壁厚度（ＬＶＡＷｄ）、左心 室射血分数（ＥＦ）。处死各组大鼠取心室肌行ＨＥ及Ｍａｓｓｏｎ染色，观察心肌病理改变。采用ｑＲＴ-ＰＣＲ法检测各组 心肌组织心肌肥厚基因［包括心房钠尿因子（ＡＮＦ）、骨骼肌肌动蛋白１（ＡＣＴＡ１）、β肌球蛋白重链］及心肌纤维化 基因［包括转化生长因子β１（ＴＧＦ-β１）、结缔组织生长因子（ＣＴＧＦ）］表达。采用Ｗｅｓｔｅｒｎｂｌｏｔ法检测各组心肌细胞 中凋亡蛋白Ｂａｘ及抗凋亡蛋白Ｂｃｌ-２蛋白的表达。采用ＴＵＮＥＬ染色法检测各组心肌细胞凋亡情况，计算凋亡指 数。结果　与假手术组相比，ＧＦＰ组ＬＶＩＤｄ增加、ＬＶＥＤＶ增加、ＬＶＡＷｄ增厚、ＥＦ降低（Ｐ＜０．０１或０．０５）；与ＧＦＰ 组相比，ｍｉＲ-４５５组ＬＶＩＤｄ降低、ＬＶＥＤＶ降低、ＬＶＡＷｄ增厚、ＥＦ增加（Ｐ＜０．０１或０．０５）。ＧＦＰ组心肌组织呈心肌 肥厚、心肌纤维化病理改变，ｍｉＲ-４５５组较ＧＦＰ组心肌肥厚、心肌纤维化病理改变明显减轻。ＧＦＰ组各心肌肥厚基 因及心肌纤维化基因ｍＲＮＡ表达均高于假手术组，ｍｉＲ-４５５组各心肌肥厚基因及心肌纤维化基因ｍＲＮＡ表达均低 于ＧＦＰ组（Ｐ＜０．０１或０．０５）。与假手术组相比，ＧＦＰ组Ｂａｘ表达增加、Ｂｃｌ-２表达降低、心肌细胞凋亡指数增高（Ｐ ＜０．０１或０．０５）；与ＧＦＰ组相比，ｍｉＲ-４５５组Ｂａｘ表达降低、Ｂｃｌ-２表达增加、心肌细胞凋亡指数降低（Ｐ＜０．０１或 ０．０５）。结论　ｍｉＲ-４５５具有抑制心室重构、改善心功能的作用，可能与其抑制心肌肥厚、心肌纤维化、心肌细胞凋 亡有关。 [ABSTRACT FROM AUTHOR]