目的 探讨侧脑室注射miR-203a-3p拮抗剂（antagomir）对脑缺血再灌注损伤（Cerebral ischemia reperfusion injury，CIRI）大鼠侧支循环重建的影响及其机制。 方法 将SD大鼠随机分为假手术组、模型组、antagomiR-NC组、antagomiR-203a-3p组，模型组、antagomiR-NC和antagomiR-203a-3p组采用线栓法构建CIRI模型；antagomiR-NC组和antagomiR-203a-3p组建模前24 h在侧脑室分别注射antagomiR-NC和miR-203a-3p antagomir，假手术组和模型组建模前24 h在侧脑室注射等量生理盐水。Zea-Longa评分评估大鼠行为学，TTC染色检测脑梗死体积，激光散斑成像技术检测侧支循环开放情况及大脑皮层微循环血流灌注量（MBPU），HE染色观察脑皮质病理学形态，RT-qPCR检测脑组织miR-203a-3p、PIK3CA、PI3K、AKT及Survivin mRNA表达，Western blot检测PIK3CA、p-PI3K、PI3K、p-AKT、AKT及Survivin蛋白表达。 结果 与模型组、antagomiR-NC组比较，antagomiR-203a-3p组大鼠神经功能缺损评分显著降低（P < 0.01），脑梗死体积明显下降（P < 0.01），可见更多侧支循环吻合支，大脑皮层MBPU显著增加（P < 0.05），脑皮质区病理损伤减轻，miR-203a-3p mRNA表达水平显著下降（P < 0.01），而PIK3CA、PI3K、Akt及Survivin mRNA的表达均显著升高（P < 0.01），PIK3CA、p-PI3K/PI3K、p-AKT/AKT及Survivin蛋白表达显著增加（P < 0.01）。 结论 抑制miR-203a-3p表达可以增加CIRI大鼠脑侧支循环开放及大脑皮层MBPU，减少病理性损伤和改善神经功能，其机制可能与miR-203a-3p antagomir激活PIK3CA/PI3K/AKT/Survivin信号通路促进侧支循环重建有关。

Objective To investigate the effect of lateral ventricle injection of miR-203a-3p antagonist（antagomir）on collateral circulation recanalization and its underlying mechanisms in rats with cerebral ischemia-reperfusion injury（CIRI）. Methods Sprague-Dawley rats were randomly allocated into four experimental groups： the sham group， the model group， the antagomiR-NC group， and the antagomiR-203a-3p group. CIRI was induced in the model， antagomiR-NC， and antagomiR-203a-3p groups using the thread embolization technique to establish the CIRI model. Twenty-four hours prior to CIRI induction， rats in the antagomiR-NC and antagomiR-203a-3p groups received a stereotaxic injection of antagomiR-NC and miR-203a-3p antagomir， respectively， into the lateral ventricle. Rats in the sham and model groups were administered an equivalent volume of sterile saline via the same route and at the same time point.Behavioral assessments were conducted using the Zea-Longa scoring system. Cerebral infarction volume was measured using TTC staining. Collateral circulation status and microcirculatory blood perfusion （MBPU） in the rat cerebral cortex were monitored using laser speckle imaging. Cortical pathological morphology was observed through hematoxylin and eosin staining. RT-qPCR was employed to analyze the expression of miR-203a-3p， PIK3CA， PI3K， AKT， and Survivin mRNA in rat brain tissue. Western blotting was employed to detect the expression of PIK3CA， p-PI3K， PI3K， p-AKT， AKT and Survivin proteins. Results In comparison to the model group and the antagomiR-NC group， rats in the miR-203a-3p group demonstrated significantly reduced neurological deficit scores， notably decreased cerebral infarct volumes，substantially more collateral circulation anastomoses could be seen， and increased MBPU in the cerebral cortex. Pathological damage in cortical regions was mitigated， with miR-203a-3p mRNA expression levels markedly decreased， while mRNA expression levels of PIK3CA， PI3K， Akt， and Survivin were significantly elevated. Correspondingly， protein expression levels of PIK3CA， p-PI3K/PI3K、p-AKT/AKT and Survivin were markedly increased. Conclusions The inhibition of miR-203a-3p expression enhances cortical MBPU and the opening of collateral circulation in rats with CIRI， thereby reducing pathological damage and improving neurological function. This mechanism may be associated with the activation of the PIK3CA/PI3K/AKT/Survivin signaling pathway by the miR-203a-3p antagomir， which facilitates the reconstruction of collateral circulation.