The therapeutic efficacy of glutamine for rats with smoking inhalation injury

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• 作者：Wuquan Li^a ; ^c ; ¹ ; Xiaochen Qiu^b ; ¹ ; Junjie Wang^a ; ¹ ; Hengyu Li^a ; ¹ ; Yu Sun^a ; Fang Zhang^a ; Haichao Jin^d ; Jinfeng Fu^c ; Zhaofan Xia^a ; ^{xiazhaofan@163.com}
• 关键词：Smoke inhalation ; Glutamine ; Heat shock proteins ; Heme oxygenase-1
• 刊名：International Immunopharmacology
• 出版年：2013
• 出版时间：June, 2013
• 年：2013
• 卷：16
• 期：2
• 页码：248-253
• 全文大小：768 K

文摘

Smoke inhalation injury represents a major cause of mortality in burn patients and is associated with a high incidence of pulmonary complications. Glutamine (GLN) is considered a conditionally essential amino acid during critical illness and injury. However, whether GLN could attenuate lung injury caused by smoke inhalation is still unknown. The purpose of this study is to investigate whether GLN has a beneficial effect on smoke inhalation induced lung injury. In our present work, rats were equally randomized into three groups: Sham group (ambient air inhalation plus GLN treatment), Control group (smoke inhalation plus physiological saline) and GLN treatment group (smoke inhalation injury plus GLN treatment). At sampling, bronchoalveolar lavage fluid was performed to determine total protein concentration and pro-inflammatory cytokine levels. Lung tissues were collected for wet/dry ratio, histopathology, hydroxyproline and Western blotting measurement. Our results exhibited that GLN attenuated the lung histopathological alterations, improved pulmonary oxygenation, and mitigated pulmonary edema. At 28 days post-injury, GLN mitigated smoke inhalation-induced excessive collagen deposition as evidence by Masson-Goldner trichrome staining and hydroxyproline content. GLN mitigated smoke inhalation-induced lung inflammatory response, and further prevented the activity of NF-kappa-B. More importantly, results from Western blotting and Immunohistochemistry exhibited that GLN enhanced the expression of HSF-1, HSP-70 and HO-1 in lung tissues. Our data demonstrated that GLN protected rats against smoke inhalation-induced lung injury and its protective mechanism seems to involve in inhibition inflammatory response and enhancing HSP expression.