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Updated: Apr 5, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell
Xiaoliang Gan1, Dandan Xing2, Guangjie Su2
1Department of Anesthesiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China ; Zhongshan Ophthalmic Center, Department of Anesthesiology, Sun Yat-sen University, Guangzhou 510060, China.
Abstract:
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.
Insights
Propofol, an antioxidant anesthetic, protects against small intestinal ischemia reperfusion injury by reducing oxidative stress and mast cell degranulation. This study shows propofol inhibits NADPH oxidase-mediated mast cell activation, mitigating injury.
Area of Science:
- Gastroenterology
- Immunology
- Pharmacology
Background:
- Small intestinal ischemia reperfusion (IIR) injury involves oxidative stress and mast cell (MC) degranulation.
- Oxidative stress is known to induce MC degranulation, exacerbating IIR.
- Propofol, an anesthetic, possesses antioxidant properties that may protect against IIR.
Purpose of the Study:
- To investigate if propofol protects against IIR injury by inhibiting oxidative stress and NADPH oxidase-mediated MC activation.
- To elucidate the role of MC degranulation in IIR and its modulation by propofol.
Main Methods:
- In vitro studies using RBL-2H3 cells treated with N-acetylcysteine (NAC) or propofol, stimulated by hydrogen peroxide (H2O2) and compound 48/80 (CP).
- Assessment of MC degranulation and its effect on small intestinal epithelial cells (IEC-6).
- In vivo studies in rats subjected to IIR, evaluating injury markers, oxidative stress, and MC degranulation, with and without NAC or propofol pretreatment.
Main Results:
- H2O2-induced MC degranulation was inhibited by NAC and propofol.
- MC degranulation aggravated H2O2-induced epithelial cell injury.
- IIR in rats increased injury markers, oxidative stress (p47phox, gp91phox, 15-F2t-Isoprostane), and MC degranulation markers (tryptase, β-hexosaminidase), while decreasing antioxidant activity (superoxide dismutase).
- Propofol and NAC pretreatment attenuated IIR injury and markers, and inhibited CP-mediated exacerbation of IIR.
Conclusions:
- Propofol confers protection against IIR injury.
- This protection is achieved by suppressing NADPH oxidase-mediated mast cell activation and subsequent oxidative stress.
- Targeting mast cell activation presents a potential therapeutic strategy for IIR.
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