Selenium-enriched Cardamine violifolia protects against sepsis-induced intestinal injury by regulating mitochondrial fusion in weaned pigs

作     者：Dan Wang Yanling Kuang Qingqing Lv Wenshuai Xie Xiao Xu Huiling Zhu Yue Zhang Xin Cong Shuiyuan Cheng Yulan Liu 

作者机构：Hubei Key Laboratory of Animal Nutrition and Feed ScienceWuhan Polytechnic UniversityWuhan 430023China Enshi Se-Run Material Engineering Technology Co.Ltd.Enshi 445000China National R&D Center for Se-rich Agricultural Products ProcessingSchool of Modern Industry for Selenium Science and EngineeringWuhan Polytechnic UniversityWuhan 430023China 

出 版 物：《中国科学:生命科学英文版》 (Science China: Life Sciences)

年 卷 期：2023年第66卷第9期

页      面：2099-2111页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China (U22A20517, 32272906 and 32102566) the Project of Wuhan Science and Technology Bureau (2022020801010391) 

主　　题：intestine MFN2 mitochondrial fusion piglets selenium sepsis 

摘      要：Sepsis is a life-threatening organ dysfunction caused by the dysregulated response of the host to an infection, and treatments are limited. Recently, a novel selenium source, selenium-enriched Cardamine violifolia(SEC) has attracted much attention due to its anti-inflammatory and antioxidant properties, but little is known about its role in the treatment of sepsis. Here, we found that SEC alleviated LPS-induced intestinal damage, as indicated by improved intestinal morphology, and increased disaccharidase activity and tight junction protein expression. Moreover, SEC ameliorated the LPS-induced release of pro-inflammatory cytokines, as indicated by decreased IL-6 level in the plasma and jejunum. Moreover, SEC improved intestinal antioxidant functions by regulating oxidative stress indicators and selenoproteins. In vitro, TNF-α-challenged IPEC-1 cells were examined and showed that selenium-enriched peptides, which are the main functional components extracted from Cardamine violifolia(CSP), increased cell viability, decreased lactate dehydrogenase activity and improved cell barrier function. Mechanistically, SEC ameliorated LPS/TNF-α-induced perturbations in mitochondrial dynamics in the jejunum and IPEC-1 cells. Moreover, CSPmediated cell barrier function is primarily dependent on the mitochondrial fusion protein MFN2 but not MFN1. Taken together,these results indicate that SEC mitigates sepsis-induced intestinal injury, which is associated with modulating mitochondrial fusion.