目的 探究益生菌Roseburia intestinalis（Ri）对心力衰竭诱导的小鼠肺损伤的保护作用。 方法 将24只C57BL/6J小鼠随机分为对照组（sham组）、模型组（TAC组）、Ri对照组（sham + Ri组）和Ri干预组（TAC + Ri组）。通过主动脉弓缩窄术（TAC）构建心力衰竭模型，术后sham组和TAC组持续每天灌胃PBS 4周，而sham+Ri组和TAC + Ri组继续接受Ri补充。采用心脏超声评估心功能变化，HE染色观察肺组织病理学改变，检测肺泡灌洗液中炎症因子水平；采用免疫组化和免疫印迹检测小鼠肺组织E-cadherin和Piezo1分布及表达。另外，选取正常人支气管上皮细胞系16HBE细胞为研究对象，采用yoda1处理以诱导Piezo1相关变化，并给予Ri干预，检测跨上皮电阻（TEER）变化、E-cadherin蛋白表达及炎症因子水平。 结果 与sham组相比，TAC组小鼠超声左心室射血分数（LVEF）和短轴缩短率（FS）显著下降（均P < 0.05），肺组织气道周围出现明显的炎性细胞浸润，肺泡灌洗液IL-6、TNF-α、IL-1β升高（均P < 0.05）；肺组织E-cadherin表达下调，Piezo1表达上调（P < 0.05）。与TAC组相比，TAC + Ri组LVEF和FS明显改善（均P < 0.05），肺组织气道周围炎症细胞浸润显著减轻，肺泡灌洗液中IL-6、TNF-α、IL-1β显著降低（P < 0.05），同时E-cadherin表达上调，Piezo1蛋白表达下调（P < 0.05）。体外实验结果显示，Yoda1处理可诱导细胞中Piezo1表达升高（P < 0.05），TEER值降低（P < 0.05）及E-cadherin表达下调（P < 0.05），并伴随炎症因子mRNA水平升高（P < 0.05）；而Ri干预可逆转上述变化。 结论 R.intestinalis可有效缓解心衰诱导的小鼠肺损伤，其作用与调控Piezo1相关信号、改善上皮屏障功能及减轻炎症反应有关。

Objective To investigate the protective effects of the probiotic Roseburia intestinalis （Ri） against lung injury induced by heart failure （HF） in mice. Methods This was an experimental study. A total of 24 C57BL/6J mice were randomly assigned to four groups： sham， transverse aortic constriction （TAC）， sham + Ri， and TAC + Ri. A heart failure model was established via transverse aortic constriction. After the surgery， the mice in the sham and TAC groups were given daily oral gavage of phosphate-buffered saline （PBS） for 4 weeks， whereas the mice in the sham + Ri and TAC + Ri groups were administered Ri. Cardiac function was evaluated through echocardiography. Lung histopathological changes were assessed using hematoxylin–eosin （HE） staining. The levels of inflammatory cytokines in bronchoalveolar lavage fluid （BALF） were measured. The expression and localization of E-cadherin and Piezo1 in lung tissues were detected by means of immunohistochemistry and Western blotting. In vitro， human bronchial epithelial 16HBE cells were treated with Yoda1 to induce Piezo1-related changes， followed by Ri intervention. Subsequently， transepithelial electrical resistance （TEER）， E-cadherin expression， and inflammatory cytokine levels were evaluated. Results Compared with the sham group， TAC mice demonstrated a significantly greater reduction in left ventricular ejection fraction （LVEF） and fractional shortening （FS） （both P < 0.05）. Concurrently， there was a notable infiltration of inflammatory cells in the peribronchial regions， along with an elevation in the levels of IL-6， TNF-α， and IL-1β in BALF （all P < 0.05）. Additionally， in the lung tissues， E-cadherin expression was down-regulated， while Piezo1 expression was up-regulated （P < 0.05）.When compared to the TAC group， TAC + Ri mice exhibited a significant improvement in LVEF and FS （both P < 0.05）. There was a reduction in pulmonary inflammatory infiltration and a decrease in the levels of IL-6， TNF-α， and IL-1β in BALF （P < 0.05）. Simultaneously， E-cadherin expression increased， and Piezo1 expression decreased （P < 0.05）.In vitro， treatment with Yoda1 led to an increase in Piezo1 expression （P < 0.05）， a decrease in TEER （P < 0.05）， a reduction in E-cadherin expression （P < 0.05）， and an elevation in the mRNA levels of inflammatory cytokines （P < 0.05）. These alterations were partially reversed by the Ri intervention. Conclusion Ri alleviates heart failure?induced lung injury in mice， potentially due to its modulation of Piezo1-related signaling， preservation of airway epithelial barrier function， and attenuation of inflammatory responses.