Low-dose erythropoietin aggravates endotoxin-induced organ damage in conscious rats |
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| Authors: | Wen-Tien Wu Tsung-Ming Hu Nien-Tsung Lin Yi-Maun Subeq Ru-Ping Lee Bang-Gee Hsu |
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| Affiliation: | 1. Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan;2. Department of Orthopedics, Tzu Chi General Hospital, Hualien, Taiwan;3. Department of Psychiatry, Yulu Veterans Hospital, Hualien, Taiwan;4. Institute of Microbiology, Immunology and Molecular Medicine, Tzu Chi University, Hualien, Taiwan;5. Department of Nursing, Tzu Chi University, Hualien, Taiwan;6. Department of Nephrology, Tzu Chi General Hospital, Hualien, Taiwan;7. School of Medicine, Tzu Chi University, Hualien, Taiwan;1. The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA;1. Maria Curie-Sk?odowska University, Faculty of Chemistry, Department of Physical Chemistry, Maria Curie-Sk?odowska Sq. 3, 20-031 Lublin, Poland;2. Medical University, Chair and Department of Medical Chemistry, Laboratory of Bioorganic Synthesis and Analysis, 4A Chod?ki Street, 20-093 Lublin, Poland;1. Departamento de Geriatría, UMAE 1 CMN del Bajío, Instituto Mexicano del Seguro Social, Hospital Aranda de la Parra, León, Guanajuato, Mexico;2. Departamento de Geriatría, UMAE 21 Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, Mexico;3. Centro de Investigaciones Biomédicas del Noreste, Instituto Mexicano del Seguro Social, León, Guanajuato, Mexico;4. Departamento de Medicina Interna, Instituto Mexicano del Seguro Social, Monterrey, Nuevo León, Mexico;5. Departamento de Posgrado, Facultad de Medicina, Centro de Investigación en Alimentos y Nutrición-FAMEN, Universidad Juárez del Estado de Durango, Durango, Mexico;6. Department of Internal Medicine, Paul L. Foster School of Medicine, Texas Tech University, El Paso, TX, United States of America;1. Department of Physiology, Diabetic Research Center, Chonbuk National University Medical School, Jeonju, Republic of Korea;2. Department of Pharmacology, Taishan Medical University, Shandong, China |
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| Abstract: | Endotoxin shock can induce the production of several inflammatory mediators such as TNF-α, IL-6, and IL-1β, leading to multiple organ dysfunction and death. Erythropoietin (EPO) has been found to interact with its receptor (EPO-R), expressed in a wide variety of non-hematopoietic tissues, to induce a range of pleiotropic cytoprotective actions. We investigated the effects of low doses of EPO (300 U/kg, intravenous administration) on the physiopathology and cytokine levels in endotoxin shock in conscious rats. Endotoxin shock was induced by intravenous injection of Escherichia coli lipopolysaccharide (20 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48 h after LPS administration. Levels of biochemical and cytokine parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), and creatine phosphokinase (CPK) were measured at 0, 1, 3, 6, 9, 12, 18, 24, and 48 h after sepsis. Serum TNF-α, IL-6, and IL-1β level was measured at 1 h after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, TNF-α, IL-6, IL-1β levels, and HR, while it decreased MAP. EPO further increased the markers of organ injury (GOT, GPT, BUN, Cre, LDH, and CPK), inflammatory biomarkers (TNF-α, IL-6, and IL-1β) and did not affect MAP and HR after LPS. EPO disserved endotoxin shock-induced liver, kidney, lung, and small intestine damage in conscious rats. In conclusion, pre-treatment with low doses of EPO increased the release of TNF-α, IL-6, and IL-1β, along with aggravating endotoxin shock-induced markers of organ injury in conscious rats. |
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