The protective effects of rapamycin on intestinal ischemia/reperfusion induced remote lung injury in mice
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概要
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Introduction: The intestinal ischemia/reperfusion (I/R) injury occurs in various clinical settings, such as mesenteric artery occlusion, trauma, and intestinal transplantation. Intestinal I/R injury elicits inflammatory responses within the intestine, including mucosal epithelial cell damage, loss of barrier function, proinflammatory cytokine production, and increased microvascular permeability. These changes develop multiple organ failure, and become fatal. However, the cure is not fully established. The mammalian target of rapamycin (mTOR) plays an important role in cellular proliferation and survival. It has been shown to be focused on a therapeutic target for various diseases such as cancer and inflammation. Herein, this study was designed to determine whether the mTOR inhibitor, rapamycin, had protective effects on intestinal I/R injury in mice. Methods: The small intestine of C57BL/6 mice was challenged with ischemia by occluding superior mesenteric artery for 1h. Rapamycin was administered intraperitoneally 1h before the induction of ischemia. In mice following intestinal I/R, the survival rate, inflammatory responses and adhesion molecules in the small intestine and lung were assessed. Bacterial cultures were performed using the homogenate samples from lungs. Phagocytic capacity in the alveolar macrophages and the activation of NF-κB in the lung were also assessed. Results: Treatment with rapamycin significantly improved survival rate after intestinal I/R. Inflammatory markers (TNF-alpha and MPO activity) in the intestinal tissue of rapamycin-treated mice were unchanged but these assays in the lung were attenuated in rapamycin-treated mice along with decreased bacterial culture and increased phagocytic capacity. The activation of NF-κB and downstream expression of adhesion molecules in the lung of rapamycin-treated mice were downregulated.Conclusion: Treatment with rapamycin improved survival rate via attenuation of intestinal I/R-induced remote lung injury.
著者
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Yoshikawa Toshikazu
Kyoto Prefectural University of Medicine
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Takagi Tomohisa
Department Of Molecular Gastroenterology And Hepatology Graduate School Of Medical Science Kyoto Pre
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Handa Osamu
Department Of Molecular Gastroenterology And Hepatology Graduate School Of Medical Science Kyoto Pre
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Uchiyama Kazuhiko
Department Of Molecular Gastroenterology And Hepatology Graduate School Of Medical Science Kyoto Pre
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Mizushima Katsura
Department Of Molecular Gastroenterology And Hepatology Kyoto Prefectural University Of Medicine
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Yagi Nobuaki
Department Of Molecular Gastroenterology And Hepatology Graduate School Of Medical Science Kyoto Pre
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Naito Yuji
Department Of Cardiovascular Center Hokkaido Social Insurance Hospital
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Kamada Kazuhiro
Department Of Gastroenterology Japanese Red Cross Kyoto Daiichi Hospital
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Ito Yoshito
Department of Media Science, Faculty of Science and Technology, Teikyo University of Science and Technology, 2525 Yatsusawa, Uenohara-machi, Kitatsuru-gun, Yamanashi 409-0193, Japan
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Katada Kazuhiro
Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan
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Iida Takaya
Department of Applied Chemistry, Nagoya Institute of Technology
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Takagi Tomohisa
Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science， Kyoto Prefectural University of Medicine
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