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18 results on '"Wu, Ya-xian"'

5. Nrf2/PHB2 alleviates mitochondrial damage and protects against Staphylococcus aureus‐induced acute lung injury

Author

Jin, Si‐Hao, primary, Sun, Jiao‐Jiao, additional, Liu, Gang, additional, Shen, Li‐Juan, additional, Weng, Yuan, additional, Li, Jin‐You, additional, Chen, Min, additional, Wang, Ying‐Ying, additional, Gao, Zhi‐Qi, additional, Jiang, Feng‐Juan, additional, Li, Sheng‐Peng, additional, Chen, Dan, additional, Pang, Qing‐Feng, additional, Wu, Ya‐Xian, additional, and Wang, Zhi‐Qiang, additional

Published
2023
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10. MiR-155-5p Attenuates Vascular Smooth Muscle Cell Oxidative Stress and Migration via Inhibiting BACH1 Expression.

Author

Tong, Ying, Zhou, Mei-Hui, Li, Sheng-Peng, Zhao, Hui-Min, Zhang, Ya-Ru, Chen, Dan, Wu, Ya-Xian, and Pang, Qing-Feng

Subjects
VASCULAR smooth muscle, MUSCLE cells, OXIDATIVE stress, CARDIOVASCULAR system, VASCULAR remodeling
Abstract

The malfunction of vascular smooth muscle cells (VSMCs) is an initiating factor in the pathogenesis of pathological vascular remodeling, including hypertension-related vascular lesions. MicroRNAs (miRNAs) have been implicated in the pathogenesis of VSMC proliferation and migration in numerous cases of cardiovascular remodeling. The evidence for the regulatory role of miR-155-5p in the development of the cardiovascular system has been emerging. However, it was previously unclear whether miR-155-5p participated in the migration of VSMCs under hypertensive conditions. Thus, we aimed to define the exact role and action of miR-155-5p in VSMC migration by hypertension. Here, we detected that the level of miR-155-5p was lower in primary VSMCs from spontaneously hypertensive rats (SHRs). Its overexpression attenuated, while its depletion accelerated, the migration and oxidative damage of VSMCs from SHRs. Our dual-luciferase reporter assay showed that miRNA-155-5p directly targeted the 3′-untranslated region (3′-UTR) of BTB and CNC homology 1 (BACH1). The miR-155-5p mimic inhibited BACH1 upregulation in SHR VSMCs. By contrast, the deletion of miR-155-5p further elevated the upregulation of BACH1 in SHR-derived VSMCs. Importantly, the overexpression of miR-155-5p and knockdown of BACH1 had synergistic effects on the inhibition of VSMCs in hypertension. Collectively, miR-155-5p attenuates VSMC migration and ameliorates vascular remodeling in SHRs, via suppressing BACH1 expression. [ABSTRACT FROM AUTHOR]

Published
2023
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11. Systematic nutrition management for locally advanced nasopharyngeal carcinoma patients undergoing radiotherapy

Author

Huang,Jian-Feng, Sun,Ren-Juan, Jiang,Wen-Jun, Wu,Ping, Zhang,Li, Xu,Mei-Qin, Zhou,Le-Yuan, Pang,Qing-Feng, Wu,Ya-Xian, Yang,Bo, and Zhang,Fu-Zheng

Subjects
nasopharyngeal carcinoma, clinical outcome, nutrition management, OncoTargets and Therapy, radiotherapy, Original Research
Abstract

Jian-Feng Huang,1,* Ren-Juan Sun,1,* Wen-Jun Jiang,1 Ping Wu,2 Li Zhang,1 Mei-Qin Xu,1 Le-Yuan Zhou,1 Qing-Feng Pang,3 Ya-Xian Wu,3 Bo Yang,1 Fu-Zheng Zhang1 1Department of Radiation Oncology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, People’s Republic of China; 2Department of Nutriology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, People’s Republic of China; 3Department of Physiopathology, Wuxi Medical School of Jiangnan University, Wuxi, Jiangsu, People’s Republic of China*These authors contributed equally to this workCorrespondence: Bo Yang; Fu-Zheng ZhangDepartment of Radiation Oncology, Affiliated Hospital of Jiangnan University, 200 Huihe Road, Wuxi 214062, People’s Republic of ChinaTel +86 510 8868 3246; +86 510 8868 2111Fax +86 510 8586 0321Email wuxiyangbo@163.com; wxsyzfz@163.comObjective: To evaluate the impact of systematic nutrition management (SNM) on nutritional status, treatment-related toxicity, quality of life (QoL), response rates, and survival in patients with locally advanced nasopharyngeal carcinoma (LA-NPC) treated by radiotherapy (RT).Methods: In this retrospective study, 56 patients with LA-NPC were selected as nutrition management group (NG) for SNM during RT till 1 month later. Another 56 patients with LA-NPC receiving RT without SNM as control group (CG) were identified from the hospital database and matched pairs with NG patients according to age, gender, stage, and body mass index (BMI) prior to RT.Results: At 1 month after RT, the percentage of malnourished patients with BMI 0.05) for the 2-year progression-free survival and overall survival (84.2% versus 79.5% and 94.7% versus 92.3%, respectively.).Conclusion: SNM for LA-NPC patients treated by RT resulted in better nutritional status, reduced treatment-related toxicity and improved QoL.Keywords: nasopharyngeal carcinoma, radiotherapy, nutrition management, clinical outcome

Published
2019

18. Protostemonine effectively attenuates lipopolysaccharide-induced acute lung injury in mice

Author

Wu, Ya-xian, He, Hui-qiong, Nie, Yun-juan, Ding, Yun-he, Sun, Lei, and Qian, Feng

Abstract

Protostemonine (PSN) is the main anti-inflammatory alkaloid extracted from the roots of Stemona sessilifolia (known as “Baibu” in traditional Chinese medicine). Here, we reported the inhibitory effects of PSN on lipopolysaccharide (LPS)-induced macrophage activation in vitro and LPS-induced acute lung injury in mice. Macrophage cell line RAW264.7 cells and mouse bone marrow-derived macrophages (BMDMs) were treated with PSN (1, 3, 10, 30 and 100 μmol/L) for 0.5 h and then challenged with LPS (0.1 μg/mL) for 24 h. Pretreatment with PSN significantly inhibited LPS-induced phosphorylation of MAPKs and AKT, iNOS expression and NO production in the macrophages. C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) to induce acute lung injury (ALI). The mice were subsequently treated with PSN (10 mg/kg, ip) at 4 and 24 h after LPS challenge. PSN administration significantly attenuated LPS-induced inflammatory cell infiltration, reduced pro-inflammatory cytokine (TNF-α, IL-1β and IL-6) production and eliminated LPS-mediated lung edema. Furthermore, PSN administration significantly inhibited LPS-induced pulmonary MPO activity. Meanwhile, LPS-induced phosphorylation of p38 MAPK, iNOS expression and NO production in the lungs were also suppressed. The results demonstrate that PSN effectively attenuates LPS-induced inflammatory responses in vitro and in vivo; the beneficial effects are associated with the decreased phosphorylation of MAPK and AKT and the reduced expression of pro-inflammatory mediators, such as iNOS, NO and cytokines. These data suggest that PSN may be a potential therapeutic agent in the treatment of ALI.

Published
2018
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