Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 7, 2022; 28(9): 918-932
Published online Mar 7, 2022. doi: 10.3748/wjg.v28.i9.918
Cystic fibrosis transmembrane conductance regulator prevents ischemia/reperfusion induced intestinal apoptosis via inhibiting PI3K/AKT/NF-κB pathway
Zhi-Wei Dong, Hui Liu, Fei-Fei Su, Xiao-Zhou Fan, Yong Zhang, Peng Liu
Zhi-Wei Dong, Department of General Surgery, Air Force Medical Center, Beijing 100000, China
Hui Liu, Department of Gastroenterology, Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Fei-Fei Su, Department of Cardiology, Air Force Medical Center, Beijing 100000, China
Xiao-Zhou Fan, Department of Ultrasound, Air Force Medical Center, Beijing 100000, China
Yong Zhang, School of Chemistry and Biological Engineering, University of Science and Technology, Beijing 100000, China
Peng Liu, Research Laboratory of Aero-Medical Support, Air Force Medical Center, Beijing 100000, China
Author contributions: Dong ZW and Liu H contributed equally to this study; Dong ZW, Liu H and Liu P designed the research; Su FF, Fan XZ, and Zhang Y conducted experiments and analyzed the data; Dong ZW and Liu H wrote the manuscript; Liu P revised the manuscript; all authors approved the final version of the article.
Supported by National Natural Science Foundation of China, No. 81800473; and "Young Eagle Project "of Air Force Medical University, No. KT2021DX007.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Air Force Medical Center.
Institutional animal care and use committee statement: All animal experiments conformed to the internationally accepted principles for the care and use of laboratory animals, No. 2020-43-YJ01.
Conflict-of-interest statement: All other authors have nothing to disclose.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Peng Liu, PhD, Research Scientist, Research Laboratory of Aero-Medical Support, Air Force Medical Center, No. 30 Fucheng Road, Haidian District, Beijing 100000, China. liupeng-81@foxmail.com
Received: November 10, 2021
Peer-review started: November 10, 2021
First decision: December 3, 2021
Revised: December 14, 2021
Accepted: January 22, 2022
Article in press: January 22, 2022
Published online: March 7, 2022
ARTICLE HIGHLIGHTS
Research background

Intestinal ischemia/reperfusion (I/R) causes local injuries in the intestine and multiple organ dysfunction syndromes or even multiple organ failure in distant organs with a mortality rate ranging from 30%–90%. The underlying mechanisms are very complex. preventing intestinal apoptosis is one of the critical targets in treating patients with intestinal I/R injury.

Research motivation

Exploring the mechanism of apoptosis in intestinal I/R injury and preventing intestinal apoptosis is one of the critical targets in treating patients with intestinal I/R injury.

Research objectives

To apoptosis and its mechanism.

Research methods

An intestinal I/R injury model was established in mice with superior mesenteric artery occlusion, and Caco2 cells were subjected to hypoxia/reoxygenation (H/R) for the simulation of I/R in vivo.

Research results

Cystic fibrosis transmembrane conductance regulator (CFTR) overexpression significantly increased the Caco2 cell viability and decreased cell apoptosis induced by the H/R. And CFTR overexpression could reverse the decreased PI3K/AKT expression induced by the I/R treatment in vivo or H/R treatment in vitro.

Research conclusions

Overexpression of CFTR attenuates H/R-induced apoptosis through PI3K/AKT/NF-κB signaling pathway in H/R-treated Caco2 cells.

Research perspectives

CFTR/PI3K/AKT/NF-κB signaling pathway is potential mechanism to protect intestinal cell from apoptosis in intestinal I/R injury and critical targets in treating patients with intestinal I/R injury.