2. Academic Validation
  3. Remote Ischemic Conditioning Relieves Necrotizing Enterocolitis Through Regulation of Redox and Inflammation

Remote Ischemic Conditioning Relieves Necrotizing Enterocolitis Through Regulation of Redox and Inflammation

  • J Interferon Cytokine Res. 2023 Apr 27. doi: 10.1089/jir.2023.0015.
Yunfei Zhang 1 2 3,  Qianyang Liu 1 2,  Kai Gao 1 2,  Bing Tian 1 2,  Hai Zhu 1 2,  Jian Liu 3,  Yuhui Hu 3,  Cuilian Ye 1 2 4,  Chunbao Guo 1 2
Affiliations

Affiliations

  • 1 Department of Pediatrics, Women and Children's Hospital, Chongqing Medical University, Chongqing, People's Republic of China.
  • 2 Department of Pediatrics, Chongqing Health Center for Women and Children, Chongqing, People's Republic of China.
  • 3 Department of Gastrointestinal Surgery, Renshou People's Hospital, Meishan, People's Republic of China.
  • 4 School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing, People's Republic of China.
PMID: 37103522 DOI: 10.1089/jir.2023.0015
Abstract

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 Grx1-/- 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 in vivo. RIC activates the PI3K/Akt/mTOR signaling pathway to control oxidative stress and inflammation. RIC might provide a new therapeutic strategy for NEC.

Keywords

PI3K; glutaredoxin-1; inflammation; necrotizing enterocolitis; redox; remote ischemic conditioning.

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