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Targeting ROS and cPLA2/COX2 Expressions Ameliorated Renal Damage in Obese Mice with Endotoxemia.
Chang, Jia-Feng; Yeh, Jih-Chen; Ho, Chun-Ta; Liu, Shih-Hao; Hsieh, Chih-Yu; Wang, Ting-Ming; Chang, Shu-Wei; Lee, I-Ta; Huang, Kuo-Yang; Wang, Jen-Yu; Lin, Wei-Ning.
Afiliação
  • Chang JF; Division of Nephrology, Department of Internal Medicine, En Chu Kong Hospital, New Taipei City 237, Taiwan. cjf6699@gamil.com.
  • Yeh JC; Renal Care Joint Foundation, New Taipei City 220, Taiwan. cjf6699@gamil.com.
  • Ho CT; Department of Nursing, Yuanpei University of Medical Technology, Hsinchu 300, Taiwan. cjf6699@gamil.com.
  • Liu SH; Graduate Institution of Biomedical and Pharmaceutical Science, College of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan. cjf6699@gamil.com.
  • Hsieh CY; Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City 235, Taiwan. cjf6699@gamil.com.
  • Wang TM; Renal Care Joint Foundation, New Taipei City 220, Taiwan. b202093012@tmu.edu.tw.
  • Chang SW; Department of Dentistry, Far Eastern Memorial Hospital, New Taipei City 220, Taiwan. b202093012@tmu.edu.tw.
  • Lee IT; Renal Care Joint Foundation, New Taipei City 220, Taiwan. earny2002@gmail.com.
  • Huang KY; Division of Pathology, En-Chu-Kong Hospital, New Taipei City 237, Taiwan. 01393@km.eck.org.tw.
  • Wang JY; Division of Nephrology, Department of Internal Medicine, En Chu Kong Hospital, New Taipei City 237, Taiwan. fish37435@Hotmail.com.
  • Lin WN; Renal Care Joint Foundation, New Taipei City 220, Taiwan. fish37435@Hotmail.com.
Int J Mol Sci ; 20(18)2019 Sep 06.
Article em En | MEDLINE | ID: mdl-31500176
Obesity is associated with metabolic endotoxemia, reactive oxygen species (ROS), chronic inflammation, and obese kidney fibrosis. Although the fat-intestine-kidney axis has been documented, the pathomechanism and therapeutic targets of obese kidney fibrosis remain unelucidated. To mimic obese humans with metabolic endotoxemia, high-fat-diet-fed mice (HF group) were injected with lipopolysaccharide (LPS) to yield the obese kidney fibrosis-metabolic endotoxemia mouse model (HL group). Therapeutic effects of ROS, cytosolic phospholipases A2 (cPLA2) and cyclooxygenase-2 (COX-2) inhibitors were analyzed with a quantitative comparison of immunohistochemistry stains and morphometric approach in the tubulointerstitium of different groups. Compared with basal and HF groups, the HL group exhibited the most prominent obese kidney fibrosis, tubular epithelial lipid vacuoles, and lymphocyte infiltration in the tubulointerstitium. Furthermore, inhibitors of nonspecific ROS, cPLA2 and COX-2 ameliorated the above renal damages. Notably, the ROS-inhibitor-treated group ameliorated not only oxidative injury but also the expression of cPLA2 and COX-2, indicating that ROS functions as the upstream signaling molecule in the inflammatory cascade of obese kidney fibrosis. ROS acts as a key messenger in the signaling transduction of obese kidney fibrosis, activating downstream cPLA2 and COX-2. The given antioxidant treatment ameliorates obese kidney fibrosis resulting from a combined high-fat diet and LPS-ROS could serve as a potential therapeutic target of obese kidney fibrosis with metabolic endotoxemia.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espécies Reativas de Oxigênio / Endotoxemia / Ciclo-Oxigenase 2 / Fosfolipases A2 Citosólicas / Nefropatias / Obesidade Limite: Animals Idioma: En Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espécies Reativas de Oxigênio / Endotoxemia / Ciclo-Oxigenase 2 / Fosfolipases A2 Citosólicas / Nefropatias / Obesidade Limite: Animals Idioma: En Ano de publicação: 2019 Tipo de documento: Article