Academic Journal

Dexmedetomidine prevents PDIA3 decrease by activating α2-adrenergic receptor to alleviate intestinal ischemia/reperfusion in mice

التفاصيل البيبلوغرافية
العنوان: Dexmedetomidine prevents PDIA3 decrease by activating α2-adrenergic receptor to alleviate intestinal ischemia/reperfusion in mice
المؤلفون: Zhan, Yaqing, Chen, Zhaorong, Qiu, Yuxin, Deng, Qiwen, Huang, Wenqi, Wen, Shihong, Shen, Jiantong
المصدر: Shock ; ISSN 1073-2322
بيانات النشر: Ovid Technologies (Wolters Kluwer Health)
سنة النشر: 2022
الوصف: Background Dexmedetomidine (DEX) attenuates intestinal ischemia/reperfusion (I/R) injury, but its mechanism of action remains to be further elucidated. Protein disulfide isomerase A3 (PDIA3) has been reported as a therapeutic protein for the prevention and treatment for intestinal I/R injury. This study was to investigate whether PDIA3 is involved in intestinal protection of DEX and explore the underlying mechanisms. Methods The potential involvement of PDIA3 in DEX attenuation of intestinal I/R injury was tested in PDIA3 Flox/Flox mice and PDIA3 conditional knockout (cKO) in intestinal epithelium mice subjected to 45 min of superior mesenteric artery (SMA) occlusion followed by 4 h of reperfusion. Furthermore, the α2-adrenergic receptor (α2-AR) antagonist, yohimbine, was administered in wild type C57BL/6 N mice intestinal I/R model to investigate the role of α2-AR in the intestinal protection conferred by DEX. Results In present study, we identified intestinal I/R induced obvious inflammation, endoplasmic reticulum (ER) stress-dependent apoptosis, and oxidative stress and all above changes were improved by the administration of DEX. PDIA3 cKO in intestinal epithelium have reversed the protective effects of DEX. Moreover, yohimbine also reversed the intestinal protection of DEX and downregulated the mRNA and protein levels of PDIA3. Conclusion DEX prevents PDIA3 decrease by activating α2-AR to inhibit intestinal I/R-induced inflammation, ER stress-dependent apoptosis and oxidative stress in mice.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1097/shk.0000000000002011
DOI: 10.1097/SHK.0000000000002011
الاتاحة: http://dx.doi.org/10.1097/shk.0000000000002011
https://journals.lww.com/10.1097/SHK.0000000000002011
Rights: http://creativecommons.org/licenses/by-nc-nd/4.0/
رقم الانضمام: edsbas.505533EE
قاعدة البيانات: BASE
الوصف
DOI:10.1097/shk.0000000000002011