https://scholars.lib.ntu.edu.tw/handle/123456789/587253
標題: | Glutamine Administration Attenuates Kidney Inflammation in Obese Mice Complicated with Polymicrobial Sepsis | 作者: | Su, Li-Han MING-TSAN LIN Yeh, Sung-Ling Yeh, Chiu-Li |
公開日期: | 2021 | 卷: | 2021 | 來源出版物: | Mediators of inflammation | 摘要: | Obesity is a well-known public health issue around the world. Sepsis is a lethal clinical syndrome that causes multiorgan failure. Obesity may aggravate inflammation in septic patients. Glutamine (GLN) is a nutrient with immune regulatory and anti-inflammatory properties. Since sepsis is a common contributing factor for acute kidney injury (AKI), this study investigated the effects of GLN administration on sepsis-induced inflammation and AKI in obese mice. A high-fat diet which consists of 60% of calories from fat was provided for 10 weeks to induce obesity in the mice. Then, the obese mice were subdivided into sepsis with saline (SS) or GLN (SG) groups. Cecal ligation and puncture (CLP) was performed to produce sepsis. The SS group was intravenously injected with saline while the SG group was administered GLN one or two doses after CLP. Obese mice with sepsis were sacrificed at 12, 24, or 48 h post-CLP. Results revealed that sepsis resulted in upregulated high-mobility group box protein-1 pathway-associated gene expression in obese mice. Also, expressions of macrophage/neutrophil infiltration markers and inflammatory cytokines in kidneys were elevated. Obese mice treated with GLN after sepsis reversed the depletion of plasma GLN, reduced production of lipid peroxides, and downregulated macrophage/neutrophil infiltration and the inflammatory-associated pathway whereas tight junction gene expression increased in the kidneys. These findings suggest that intravenously administered GLN to obese mice after sepsis alleviated inflammation and attenuated AKI. This model may have clinical application to obese patients with a risk for infection in abdominal surgery. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/587253 | ISSN: | 09629351 | DOI: | 10.1155/2021/5597118 | SDG/關鍵字: | alanylglutamine; biochemical marker; CD68 antigen; cytokine; glutamine; hepatitis A virus cellular receptor 1; high mobility group B1 protein; interleukin 10; keratinocyte derived chemokine; lipid peroxide; malonaldehyde; messenger RNA; monocyte chemotactic protein 1; myeloid differentiation factor 88; myeloperoxidase; neutrophil gelatinase associated lipocalin; protein ZO1; sodium chloride; thiobarbituric acid reactive substance; toll like receptor 4; tumor necrosis factor; amino acid; glutamine; high mobility group B1 protein; HMGB1 protein, mouse; acute kidney failure; adult; amino acid blood level; animal experiment; animal model; animal tissue; Article; cecal ligation and puncture-induced sepsis; controlled study; down regulation; gene expression; male; mouse; mRNA expression level; nephritis; neutrophil chemotaxis; nonhuman; obesity; protein blood level; protein expression; sepsis; signal transduction; single drug dose; tight junction; upregulation; acute kidney failure; animal; blood; C57BL mouse; complication; inflammation; lipid diet; metabolism; mouse mutant; obesity; physiology; sepsis; Acute Kidney Injury; Amino Acids; Animals; Diet, High-Fat; Glutamine; HMGB1 Protein; Inflammation; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Sepsis |
顯示於: | 醫學系 |
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