Department of Pediatrics, Women and Children's Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
Department of Pediatrics, Chongqing Health Center for Women and Children, Chongqing, People's Republic of China.
J Interferon Cytokine Res. 2023 May;43(5):216-228. doi: 10.1089/jir.2023.0015. Epub 2023 Apr 27.
In neonates, necrotizing enterocolitis (NEC) is a serious condition involving oxidative stress and inflammation. Remote ischemic conditioning (RIC) is a potentially useful technique to protect distant organs from the damage induced by ischemia. RIC has been verified as effective to protect against NEC; however, its mechanism is unclear. This study aimed to assess the mechanism and efficacy of RIC to treat experimental NEC in mice. Between postnatal day (P) 5 and P9, we induced NEC in C57BL/6 mice and mice. Intermittent occlusion of the blood flow to the right hind limb for 4 cycles of 5 min ischemia followed by 5 min reperfusion during NEC induction on P6 and P8 was used to apply RIC. We sacrificed the mice on p9 and evaluated oxidative stress, inflammatory cytokines, proliferation, apoptosis, and PI3K/Akt/mTOR signal pathway in mice ileal tissue. RIC decreased intestinal injury and prolonged survival in NEC pups. RIC significantly inhibited inflammatory, attenuated oxidative stress, reduced apoptosis, promoted proliferation, and activated PI3K/Akt/mTOR . RIC activates the PI3K/Akt/mTOR signaling pathway to control oxidative stress and inflammation. RIC might provide a new therapeutic strategy for NEC.
在新生儿中，坏死性小肠结肠炎（NEC）是一种涉及氧化应激和炎症的严重疾病。远程缺血预处理（RIC）是一种保护远隔器官免受缺血引起的损伤的潜在有用技术。RIC 已被证实对预防 NEC 有效，但其机制尚不清楚。本研究旨在评估 RIC 治疗实验性 NEC 小鼠的机制和疗效。在出生后第 5 天至第 9 天，我们在 C57BL/6 小鼠和 小鼠中诱导 NEC。在 P6 和 P8 诱导 NEC 时，对右后肢血流进行 4 个周期的 5 分钟缺血，随后进行 5 分钟再灌注，以应用 RIC。我们在第 9 天处死小鼠，并评估小鼠回肠组织中的氧化应激、炎症细胞因子、增殖、凋亡和 PI3K/Akt/mTOR 信号通路。RIC 可减轻 NEC 幼鼠的肠道损伤并延长其存活时间。RIC 显著抑制炎症、减轻氧化应激、减少凋亡、促进增殖并激活 PI3K/Akt/mTOR 。RIC 通过激活 PI3K/Akt/mTOR 信号通路来控制氧化应激和炎症。RIC 可能为 NEC 提供一种新的治疗策略。
