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<p>Anastomotic stricture is the most common complication after esophageal surgery, often linked to inflammation. Prior work showed that remote ischemic conditioning (RIC) alleviates strictures by reducing inflammation. This study investigated whether RIC’s effectiveness is also associated with angiogenesis and cell proliferation after esophageal resection and anastomosis (R&amp;A). Sixty-five Sprague–Dawley rats underwent cervical esophageal R&amp;A and were divided into three groups: R&amp;A only (<i>n</i> = 20), R&amp;A with one session of RIC (RIC1, <i>n</i> = 20), and R&amp;A with two sessions of RIC (RIC2, <i>n</i> = 20). RIC involved three cycles of 5-minute ischemia/reperfusion on the left hind limb. On postoperative day 7, stricture severity was assessed radiographically. Histological and molecular analyses (immunohistochemistry, Western blotting) evaluated markers for angiogenesis (e.g., cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF)) and cell proliferation (e.g., Kiel 67 (Ki67), cyclin-dependent kinase 6, p21). RIC treatment significantly promoted angiogenesis, evidenced by increased vessel density and elevated expression of CD31 and VEGF in both RIC groups. Western blot analysis showed significant activation of the PI3K/Akt pathway in the RIC1 group. Importantly, RIC enhanced cell proliferation, indicated by a significant increase in Ki67 expression. This proliferative effect was confirmed by increased cell cycle regulators (cyclin-dependent kinase 6, cyclin A) and a reduction in inhibitors (p21, p27) in the RIC groups. This study demonstrates that applying RIC after esophageal R&amp;A promotes angiogenesis and increases proliferation through cell cycle activation. These biological modulations contribute to the improvement of anastomotic strictures, suggesting RIC is a key modulator of the stricture formation and recovery process.</p>

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Enhanced angiogenetic and proliferative effects of remote ischemic conditioning following esophageal resection and anastomosis in a rat model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月6日

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  • Joong Kee Youn,
  • Hye-Rim Lee,
  • So-Young Kim,
  • Dayoung Ko,
  • Hyun-Young Kim

摘要

Anastomotic stricture is the most common complication after esophageal surgery, often linked to inflammation. Prior work showed that remote ischemic conditioning (RIC) alleviates strictures by reducing inflammation. This study investigated whether RIC’s effectiveness is also associated with angiogenesis and cell proliferation after esophageal resection and anastomosis (R&A). Sixty-five Sprague–Dawley rats underwent cervical esophageal R&A and were divided into three groups: R&A only (n = 20), R&A with one session of RIC (RIC1, n = 20), and R&A with two sessions of RIC (RIC2, n = 20). RIC involved three cycles of 5-minute ischemia/reperfusion on the left hind limb. On postoperative day 7, stricture severity was assessed radiographically. Histological and molecular analyses (immunohistochemistry, Western blotting) evaluated markers for angiogenesis (e.g., cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF)) and cell proliferation (e.g., Kiel 67 (Ki67), cyclin-dependent kinase 6, p21). RIC treatment significantly promoted angiogenesis, evidenced by increased vessel density and elevated expression of CD31 and VEGF in both RIC groups. Western blot analysis showed significant activation of the PI3K/Akt pathway in the RIC1 group. Importantly, RIC enhanced cell proliferation, indicated by a significant increase in Ki67 expression. This proliferative effect was confirmed by increased cell cycle regulators (cyclin-dependent kinase 6, cyclin A) and a reduction in inhibitors (p21, p27) in the RIC groups. This study demonstrates that applying RIC after esophageal R&A promotes angiogenesis and increases proliferation through cell cycle activation. These biological modulations contribute to the improvement of anastomotic strictures, suggesting RIC is a key modulator of the stricture formation and recovery process.