Dexmedetomidine protects against sepsis-induced lung injury through autophagy and Smad2/3 signaling pathway | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 7، دوره 27، شماره 4، تیر 2024، صفحه 453-460 اصل مقاله (782.38 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2023.73479.15964 | ||
| نویسندگان | ||
| Zhanli Liu1؛ Jiqing Xu2؛ Yanqiu Zhao3؛ Yanbin Wan3؛ Rui Guo3؛ Canling Long3؛ Jia Liu3؛ Xinhuang Yao* 3؛ Wenchao Yin* 4 | ||
| 1Department of Anesthesiology, Shenzhen People’s Hospital and Shenzhen Anesthesiology Engineering Center, the Second Clinical Medical College of Jinan University, Shenzhen, China | ||
| 2Department of Cardiothoracic Surgery, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, China | ||
| 3Central Laboratory, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People’s Hospital of Shenzhen, Shenzhen, China | ||
| 4Department of Anesthesiology, Sichuan Provincial Orthopedic Hospital, Chengdu, China | ||
| چکیده | ||
| Objective(s): Dexmedetomidine (Dex) is a potent α2-adrenergic receptor(α2-AR) agonist that has been shown to protect against sepsis-induced lung injury, however, the underlying mechanisms of this protection are not fully understood. Autophagy and the Smad2/3 signaling pathway play important roles in sepsis-induced lung injury, but the relationship between Dex and Smad2/3 is not clear. This study aimed to investigate the role of autophagy and the Smad2/3 signaling pathway in Dex-mediated treatment of sepsis-induced lung injury. Sepsis was performed using cecal ligation and puncture (CLP) in C57BL/6J mice. Materials and Methods: Mice were randomly assigned to four groups (n=6 per group): sham, CLP, CLP-Dex, and CLP-Dex-YOH, Yohimbine hydrochloride (YOH) is an α2-AR blocker. The cecum was carefully separated to avoid blood vessel damage and was identified and punctured twice with an 18-gauge needle. The pathological changes, inflammatory factor levels, oxidative stress, autophagy, Smad2/3 signaling pathway-related protein levels in lung tissues, and the activity of superoxide dismutase (SOD) and malonaldehyde (MDA) in the serum were measured. Results: CLP-induced lung injury was reflected by increased levels of inflammatory cytokines, apoptosis, and oxidative stress, along with an increase in the expression of autophagy and Smad2/3 signaling pathway-related proteins. Dex could reverse these changes and confer a protective effect on the lung during sepsis. However, the administration of YOH significantly reduced the positive effects of Dex in mice with sepsis. Conclusion: Dex exerts its beneficial effects against sepsis-induced lung injury through the regulation of autophagy and the Smad2/3 signaling pathway. | ||
| کلیدواژهها | ||
| Acute lung injury؛ Autophagy؛ Dexmedetomidine؛ Sepsis؛ Smad2/3 | ||
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