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Updated: Jun 26, 2025
Analyzing Oxidative Stress in Murine Intestinal Organoids using Reactive Oxygen Species-Sensitive Fluorogenic Probe
Published on: September 17, 2021
ROS-responsive carboxymethyl chitosan nanoparticles loaded with astaxanthin for alleviating oxidative damage in
Xiaoting Yu1, Yannan Chen1, Mingqian Tan1
1State Key Laboratory of Marine Food Processing and Safety Control, Dalian Polytechnic University, Dalian, Liaoning 116034, China; Academy of Food Interdisciplinary Science, School of Food Science and Technology, Dalian Polytechnic University, Dalian, Liaoning 116034, China; National Engineering Research Center of Seafood, Dalian Polytechnic University, Dalian, Liaoning 116034, China; Collaborative Innovation Center of Seafood Deep Processing, Dalian Polytechnic University, Dalian, Liaoning 116034, China; Dalian Key Laboratory for Precision Nutrition, Dalian Polytechnic University, Dalian, Liaoning 116034, China.
Abstract:
The controlled release of antioxidant substances at the intestinal oxidative damage site is crucial for alleviating intestine-related diseases. Herein, the novel ROS-responsive carrier was synthesized through simple amidation reaction between carboxymethyl chitosan (CMC) and methionine (Met), a natural organic compound containing ROS-responsive linkages (thioether). Initially, astaxanthin (AXT) nanoparticles (AXT2@CMT) with excellent stability and drug loading capacity (39.68 ± 0.23 μg/mL) were prepared by optimizing various reaction conditions. In the simulated high-concentration ROS environment of the intestine, CMT achieved a transition from hydrophobic groups (thioether) into hydrophilic groups (sulfone), which was conducive to the controlled release of AXT. In vitro cell experiments revealed that AXT2@CMT could effectively alleviate the oxidative damage in intestinal epithelioid cell line No. 6 (IEC-6 cell) caused by H2O2. This study achieved a straightforward preparation of ROS-responsive nanocarrier through food ingredients, offering a theoretical foundation for the controlled release of AXT at the intestinal oxidative damage site.
