Lipopolysaccharides protect mesenchymal stem cell against cardiac ischemia-reperfusion injury by HMGB1/STAT3 sig-naling
Jing-Yi WEN1
Hui-Xi PENG2
Dan WANG3
Zhi-Min WEN4
Yu-Tong LIU4
Jian QU4
Hong-Xuan CUI2
Yu-Ying WANG2
Yan-Lin DU2
Ting WANG4
Cong GENG4
Bing XU2
1.Department of Clinical Pharmacy,the Second Affiliated Hospital of Dalian Medical University,Dalian,Liaoning,China;Department of Pharmacy,the Second Affiliated Hospital of Inner Mongolia Medical University,Hohhot,Inner Mongolia,China2.Department of Clinical Pharmacy,the Second Affiliated Hospital of Dalian Medical University,Dalian,Liaoning,China3.Department of Pharmacy,Ordos Central Hospital,Ordos,Inner Mongolia,China4.Department of Clinical Laboratory,the Second Affiliated Hospital of Dalian Medical University,Dalian,Liaoning,China
摘要：BACKGROUND Myocardial ischemia-reperfusion(I/R)is a serious and irreversible injury.Bone marrow-derived mesenchy-mal stem cells(MSCs)is considered to be a potential therapy for I/R injury due to the paracrine effects.High-mobility group box 1(HMGB1)is a novel mediator in MSC and regulates the response of inflammation injury.Signal Transduction and Transcrip-tion Activator 3(STAT3)is a critical transcription factor and important for release of paracrine factors.However,the relationship between HMGB1 and STAT3 in paracrine effect of MSC remains unknown.
METHODS In vitro,hypoxia/reoxygenation injury model was established by AnaeroPack System and examined by Annexin V flow cytometry,CCK8 assay and morphology observation.Detection of apoptotic proteins and protein expression of HMGB1
RESULTS The conditioned medium of MSCs with or without LPS pretreatment was cocultured with H9C2 cells for 24 h be-fore hypoxia treatment and MSC showed obvious cardiomyocytes protect role,as evidence by decreased apoptosis rate and im-proved cells viability,and LPS pretreated MSC exhibited better protect role than untreated MSC.However,such effect was abol-ished in HMGB1 deficiency group,silencing HMGB1 decreased the secretion of vascular endothelial growth factor(VEGF),hep-atocyte growth factor(HGF),insulin growth factor(IGF),cell viability,and the expression of STAT3.Furthermore,STAT3 silence attenuated the protective effect of LPS in MSC.
CONCLUSIONS These findings suggested that LPS improved MSC-mediated cardiomyocytes protection by HMGB1/STAT3 signaling.
机标关键词：polysaccharidesstat3ischemiahmgb1stemlipopcellopol
论文发表日期：2023-11-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：12( 801-812 )