Corrigendum to 'Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation'
Autor: | Dandan Xing, Zhengyuan Xia, Haobo Li, Guangjie Su, Xiaoliang Gan, Chenfang Luo, Shun Li, Ziqing Hei, Michael G. Irwin |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Aging Cell Survival 030204 cardiovascular system & hematology Pharmacology Biochemistry Antioxidants Cell Degranulation Cell Line Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Animals p-Methoxy-N-methylphenethylamine Medicine Mast Cells lcsh:QH573-671 Intestinal Mucosa Propofol Membrane Glycoproteins NADPH oxidase biology lcsh:Cytology business.industry Mast cell activation Intestinal ischemia NADPH Oxidases Hydrogen Peroxide Cell Biology General Medicine medicine.disease beta-N-Acetylhexosaminidases Acetylcysteine Rats Up-Regulation Oxidative Stress 030104 developmental biology Reperfusion Injury Anesthesia NADPH Oxidase 2 biology.protein Female Tryptases Corrigendum business Reperfusion injury medicine.drug |
Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2017 (2017) |
ISSN: | 1942-0994 1942-0900 |
DOI: | 10.1155/2017/8932871 |
Popis: | Both oxidative stress and mast cell (MC) degranulation participate in the process of small intestinal ischemia reperfusion (IIR) injury, and oxidative stress induces MC degranulation. Propofol, an anesthetic with antioxidant property, can attenuate IIR injury. We postulated that propofol can protect against IIR injury by inhibiting oxidative stress subsequent from NADPH oxidase mediated MC activation. Cultured RBL-2H3 cells were pretreated with antioxidant N-acetylcysteine (NAC) or propofol and subjected to hydrogen peroxide (H2O2) stimulation without or with MC degranulator compound 48/80 (CP). H2O2 significantly increased cells degranulation, which was abolished by NAC or propofol. MC degranulation by CP further aggravated H2O2 induced cell degranulation of small intestinal epithelial cell, IEC-6 cells, stimulated by tryptase. Rats subjected to IIR showed significant increases in cellular injury and elevations of NADPH oxidase subunits p47(phox) and gp91(phox) protein expression, increases of the specific lipid peroxidation product 15-F2t-Isoprostane and interleukin-6, and reductions in superoxide dismutase activity with concomitant enhancements in tryptase and β-hexosaminidase. MC degranulation by CP further aggravated IIR injury. And all these changes were attenuated by NAC or propofol pretreatment, which also abrogated CP-mediated exacerbation of IIR injury. It is concluded that pretreatment of propofol confers protection against IIR injury by suppressing NADPH oxidase mediated MC activation. |
Databáze: | OpenAIRE |
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