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Effect of dexmedetomidine on endoplasmic reticulum stress during intestinal ischemia-reperfusion in mice

Zhilu Pang, Zhijie Fu, Long He, Mingzhu Cui, Jiaqiang Zhang

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Abstract

Objective To evaluate the effect of dexmedetomidine on endoplasmic reticulum stress during intestinal ischemia-reperfusion(I/R)in mice. Methods Thirty SPF healthy male C57BL/6 mice, aged 8 weeks, were divided into 3 groups(n=10 each)using a random number table method: sham operation group(S group), intestinal I/R group(I/R group)and dexmedetomidine group(DEX group). The superior mesenteric artery was only isolated but not clamped in S group.The model of intestinal I/R injury was established by clamping superior mesenteric artery for 20 min followed by 24 h of reperfusion in I/R group and DEX group.Dexmedetomidine 25 μg/kg was intraperitoneally injected at 30 min before ischemia in DEX group, while the equal volume of normal saline was given instead of dexmedetomidine in S group and I/R group.Mice were sacrificed at 24 h of reperfusion, and small intestinal tissues was obtained for examination of the pathological changes and ultrastructure of intestinal epithelial cells and for determination of cell apoptosis, expression of CCAAT-enhancer binding protein homologous protein(CHOP), transcription factors(ATF4), and X-4 box binding protein 1(XBP1)mRNA(by real-time polymerase chain reaction), and expression of CHOP, Bcl-2, Bax and caspase-3 in intestinal tissues(by Western bolt). The apoptosis index(AI)and ratio of Bcl-2 to Bax were calculated.Intestinal damage was assessed and scored according to Chiu. Results Compared with S group, Chiu′s score and AI were significantly increased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was up-regulated, and the expression of Bcl-2 was down-regulated, and Bcl-2/Bax ratio was decreased in I/R group and DEX group(P<0.05). Compared with I/R group, Chiu′s score and AI were significantly decreased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was down-regulated, and the expression of Bcl-2 was up-regulated, and Bcl-2/Bax ratio was increased in DEX group(P<0.05). Conclusion The mechanism by which dexmedetomidine reduces intestinal I/R injury may be related to regulating endoplasmic reticulum stress and inhibiting cell apoptosis in mice. Key words: Dexmedetomidine; Intestines; Reperfusion injury; Endoplasmic reticulum; Stress

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Objective To evaluate the effect of dexmedetomidine on endoplasmic reticulum stress during intestinal ischemia-reperfusion(I/R)in mice. Methods Thirty SPF healthy male C57BL/6 mice, aged 8 weeks, were divided into 3 groups(n=10 each)using a random number table method: sham operation group(S group), intestinal I/R group(I/R group)and dexmedetomidine group(DEX group). The superior mesenteric artery was only isolated but not clamped in S group.The model of intestinal I/R injury was established by clamping superior mesenteric artery for 20 min followed by 24 h of reperfusion in I/R group and DEX group.Dexmedetomidine 25 μg/kg was intraperitoneally injected at 30 min before ischemia in DEX group, while the equal volume of normal saline was given instead of dexmedetomidine in S group and I/R group.Mice were sacrificed at 24 h of reperfusion, and small intestinal tissues was obtained for examination of the pathological changes and ultrastructure of intestinal epithelial cells and for determination of cell apoptosis, expression of CCAAT-enhancer binding protein homologous protein(CHOP), transcription factors(ATF4), and X-4 box binding protein 1(XBP1)mRNA(by real-time polymerase chain reaction), and expression of CHOP, Bcl-2, Bax and caspase-3 in intestinal tissues(by Western bolt). The apoptosis index(AI)and ratio of Bcl-2 to Bax were calculated.Intestinal damage was assessed and scored according to Chiu. Results Compared with S group, Chiu′s score and AI were significantly increased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was up-regulated, and the expression of Bcl-2 was down-regulated, and Bcl-2/Bax ratio was decreased in I/R group and DEX group(P<0.05). Compared with I/R group, Chiu′s score and AI were significantly decreased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was down-regulated, and the expression of Bcl-2 was up-regulated, and Bcl-2/Bax ratio was increased in DEX group(P<0.05). Conclusion The mechanism by which dexmedetomidine reduces intestinal I/R injury may be related to regulating endoplasmic reticulum stress and inhibiting cell apoptosis in mice. Key words: Dexmedetomidine; Intestines; Reperfusion injury; Endoplasmic reticulum; Stress

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Available abstract

Objective To evaluate the effect of dexmedetomidine on endoplasmic reticulum stress during intestinal ischemia-reperfusion(I/R)in mice. Methods Thirty SPF healthy male C57BL/6 mice, aged 8 weeks, were divided into 3 groups(n=10 each)using a random number table method: sham operation group(S group), intestinal I/R group(I/R group)and dexmedetomidine group(DEX group). The superior mesenteric artery was only isolated but not clamped in S group.The model of intestinal I/R injury was established by clamping superior mesenteric artery for 20 min followed by 24 h of reperfusion in I/R group and DEX group.Dexmedetomidine 25 μg/kg was intraperitoneally injected at 30 min before ischemia in DEX group, while the equal volume of normal saline was given instead of dexmedetomidine in S group and I/R group.Mice were sacrificed at 24 h of reperfusion, and small intestinal tissues was obtained for examination of the pathological changes and ultrastructure of intestinal epithelial cells and for determination of cell apoptosis, expression of CCAAT-enhancer binding protein homologous protein(CHOP), transcription factors(ATF4), and X-4 box binding protein 1(XBP1)mRNA(by real-time polymerase chain reaction), and expression of CHOP, Bcl-2, Bax and caspase-3 in intestinal tissues(by Western bolt). The apoptosis index(AI)and ratio of Bcl-2 to Bax were calculated.Intestinal damage was assessed and scored according to Chiu. Results Compared with S group, Chiu′s score and AI were significantly increased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was up-regulated, and the expression of Bcl-2 was down-regulated, and Bcl-2/Bax ratio was decreased in I/R group and DEX group(P<0.05). Compared with I/R group, Chiu′s score and AI were significantly decreased, the expression of CHOP, ATF4 and XBP-1 mRNA, CHOP, Bax and caspase-3 was down-regulated, and the expression of Bcl-2 was up-regulated, and Bcl-2/Bax ratio was increased in DEX group(P<0.05). Conclusion The mechanism by which dexmedetomidine reduces intestinal I/R injury may be related to regulating endoplasmic reticulum stress and inhibiting cell apoptosis in mice. Key words: Dexmedetomidine; Intestines; Reperfusion injury; Endoplasmic reticulum; Stress

Key concepts: Dexmedetomidine, CHOP, Apoptosis, Endoplasmic reticulum, Superior mesenteric artery, Reperfusion injury, Ischemia, Endocrinology

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