Exosomes of Antler Mesenchymal Stem Cells Improve Postoperative Cognitive Dysfunction in Cardiopulmonary Bypass Rats through Inhibiting the TLR2/TLR4 Signaling Pathway

Stem Cells International

Tengfei Wu¹  Min Yang²  Qi Zhang²  Chun Yang²  Ying Liu²  Shengnan Sun²  Jia Guo²  Yinghua Peng²  Yan Zhang³ 

[1] Department of Laboratory Animal Science, China Medical University, Shenyang, China, cmu.edu.cn;Institute of Special Wild Economic Animal and Plants, Chinese Academy of Agricultural Sciences, Changchun, China, caas.net.cn;State Key Laboratory for Molecular Biology of Special Economic Animal, Changchun, China;Key Laboratory of Jilin Province for Zoonosis Prevention and Control, Institute of Military Veterinary, Academy of Military Medical Sciences, Changchun, China, bmi.ac.cn;

DOI  :  10.1155/2020/2134565

来源: publisher

【 摘 要 】

Postoperative cognitive dysfunction (POCD) is a severe complication of cardiopulmonary bypass (CPB) and has common characteristics such as acute cognitive dysfunction, impaired memory, and inattention. Mesenchymal stem cells (MSCs) are multipotent cells that have therapeutic potentials mainly through paracrine action via secreting growth factors and cytokines. Exosomes are one of the important paracrine factors and have been reported as potential cell-free therapy for the treatment of autoimmune and central nervous system disorders. In this study, we examined exosomes derived from antler MSCs (AMSCs) of POCD rats after CPB and evaluated their potential regulatory mechanisms. AMSC-derived exosomes reduced neurological damage and brain damage and prevent apoptosis in CPB rats. Furthermore, AMSC-derived exosomes were found to reduce hippocampal neuronal apoptosis and the expression of TLR2, TLR4, MyD88, and NF-κB in CPB rats. However, the above effects of AMSC-derived exosomes on CPB rats were abolished partially by toll-like receptor 2/4 (TLR2/TLR4) agonist (LPS-EB). In conclusion, AMSC-derived exosomes can improve cognitive function in CPB rats through inhibiting the TLR2/TLR4 signaling pathway.

【 授权许可】

Unknown