Search

Your search keyword '"Song, Ji‐Xian"' showing total 10 results
Start Over Author "Song, Ji‐Xian"
10 results on '"Song, Ji‐Xian"'

4. Cardiomyocyte‐specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia.

Author

Song, Ji‐Xian, Xu, Shan, Chen, Qi, Gou, Yujing, Zhao, Chen‐Bing, Jia, Cui‐Ling, Liu, Han, Zhang, Zhi, Li, Bo‐liang, Gao, Yuhui, Zhao, Yashuo, and Ji, En‐Sheng

Subjects
CARDIAC hypertrophy, HEART diseases, HEPCIDIN, GENETIC overexpression, IRON
Abstract

The significance of iron in myocardial mitochondria function cannot be underestimated, because deviations in iron levels within cardiomyocytes may have profound detrimental effects on cardiac function. In this study, we investigated the effects of ferroportin 1 (FPN1) on cardiac iron levels and pathological alterations in mice subjected to chronic intermittent hypoxia (CIH). The cTNT‐FPN1 plasmid was administered via tail vein injection to induce the mouse with FPN1 overexpression in the cardiomyocytes. CIH was established by exposing the mice to cycles of 21%–5% FiO2 for 3 min, 8 h per day. Subsequently, the introduction of hepcidin resulted in a reduction in FPN1 expression, and H9C2 cells were used to establish an IH model to further elucidate the role of FPN1. First, FPN1 overexpression ameliorated CIH‐induced cardiac dysfunction, myocardial hypertrophy, mitochondrial damage and apoptosis. Second, FPN1 overexpression attenuated ROS levels during CIH. In addition, FPN1 overexpression mitigated CIH‐induced cardiac iron accumulation. Moreover, the administration of hepcidin resulted in a reduction in FPN1 levels, further accelerating the CIH‐induced levels of ROS, LIP and apoptosis in H9C2 cells. These findings indicate that the overexpression of FPN1 in cardiomyocytes inhibits CIH‐induced cardiac iron accumulation, subsequently reducing ROS levels and mitigating mitochondrial damage. Conversely, the administration of hepcidin suppressed FPN1 expression and worsened cardiomyocyte iron toxicity injury. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

6. Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia

Author

Yang,Xin-Yue, Geng,Lina, Li,Ronghui, Song,Ji-Xian, Jia,Cui-Ling, An,Ji-Ren, Sun,Meng-Fan, Xu,Shan, Guo,Ya-Jing, Zhao,Yashuo, Ji,En-Sheng, Yang,Xin-Yue, Geng,Lina, Li,Ronghui, Song,Ji-Xian, Jia,Cui-Ling, An,Ji-Ren, Sun,Meng-Fan, Xu,Shan, Guo,Ya-Jing, Zhao,Yashuo, and Ji,En-Sheng

Abstract

Xin-Yue Yang,1,* Lina Geng,2,* Ronghui Li,2 Ji-Xian Song,1 Cui-Ling Jia,1 Ji-Ren An,1,3 Meng-Fan Sun,1 Shan Xu,1 Ya-Jing Guo,1 Yashuo Zhao,1 En-Sheng Ji1 1Hebei Technology Innovation Center of TCM Combined Hydrogen Medicine, Hebei University of Chinese Medicine, Shijiazhuang, People’s Republic of China; 2College of Chemistry and Material Science, Hebei Normal University, Shijiazhuang, People’s Republic of China; 3The First Clinical College, Liaoning University of Traditional Chinese Medicine, Shenyang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yashuo Zhao; En-Sheng Ji, No. 3, Luqian Xingyuan Road, Shijiazhuang, 050200, People’s Republic of China, Email zys870207@126.com; jesphy@126.comBackground: Chronic intermittent hypoxia (CIH) could cause neuronal damage, accelerating the progression of dementia. However, safe and effective therapeutic drugs and delivery are needed for successful CIH therapy.Purpose: To investigate the neuroprotective effect of Huperzine A (HuA) packaged with nanoliposomes (HuA-LIP) on neuronal damage induced by CIH.Methods: The stability and release of HuA-LIP in vitro were identified. Mice were randomly divided into the Control, CIH, HuA-LIP, and HuA groups. The mice in the HuA and HuA-LIP groups received HuA (0.1 mg/kg, i.p.), and HuA-LIP was administered during CIH exposure for 21 days. HuA-LIP contains the equivalent content of HuA.Results: We prepared a novel formulation of HuA-LIP that had good stability and controlled release. First, HuA-LIP significantly ameliorated cognitive dysfunction and neuronal damage in CIH mice. Second, HuA-LIP elevated T-SOD and GSH-Px abilities and decreased MDA content to resist oxidative stress damage induced by CIH. Furthermore, HuA-LIP reduced brain iron levels by downregulating TfR1, hepcidin, and FTL expression. In addition, HuA-LIP activated the PKAα/Erk/CREB/BDNF signaling pathway and elevated MAP2, PSD95, and synaptophysin

Published
2023

Catalog

Books, media, physical & digital resources
See catalog results