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Low-dose erythropoietin aggravates endotoxin-induced organ damage in conscious rats.
Cytokine. 2010 Feb; 49(2):155-62.C

Abstract

Endotoxin shock can induce the production of several inflammatory mediators such as TNF-alpha, IL-6, and IL-1beta, 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 (300U/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 (20mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48h 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 48h after sepsis. Serum TNF-alpha, IL-6, and IL-1beta level was measured at 1h after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, TNF-alpha, IL-6, IL-1beta 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-alpha, IL-6, and IL-1beta) 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-alpha, IL-6, and IL-1beta, along with aggravating endotoxin shock-induced markers of organ injury in conscious rats.

Authors+Show Affiliations

Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20004111

Citation

Wu, Wen-Tien, et al. "Low-dose Erythropoietin Aggravates Endotoxin-induced Organ Damage in Conscious Rats." Cytokine, vol. 49, no. 2, 2010, pp. 155-62.
Wu WT, Hu TM, Lin NT, et al. Low-dose erythropoietin aggravates endotoxin-induced organ damage in conscious rats. Cytokine. 2010;49(2):155-62.
Wu, W. T., Hu, T. M., Lin, N. T., Subeq, Y. M., Lee, R. P., & Hsu, B. G. (2010). Low-dose erythropoietin aggravates endotoxin-induced organ damage in conscious rats. Cytokine, 49(2), 155-62. https://doi.org/10.1016/j.cyto.2009.11.002
Wu WT, et al. Low-dose Erythropoietin Aggravates Endotoxin-induced Organ Damage in Conscious Rats. Cytokine. 2010;49(2):155-62. PubMed PMID: 20004111.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Low-dose erythropoietin aggravates endotoxin-induced organ damage in conscious rats. AU - Wu,Wen-Tien, AU - Hu,Tsung-Ming, AU - Lin,Nien-Tsung, AU - Subeq,Yi-Maun, AU - Lee,Ru-Ping, AU - Hsu,Bang-Gee, Y1 - 2009/12/08/ PY - 2009/04/04/received PY - 2009/09/10/revised PY - 2009/11/05/accepted PY - 2009/12/17/entrez PY - 2009/12/17/pubmed PY - 2010/4/13/medline SP - 155 EP - 62 JF - Cytokine JO - Cytokine VL - 49 IS - 2 N2 - Endotoxin shock can induce the production of several inflammatory mediators such as TNF-alpha, IL-6, and IL-1beta, 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 (300U/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 (20mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48h 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 48h after sepsis. Serum TNF-alpha, IL-6, and IL-1beta level was measured at 1h after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, TNF-alpha, IL-6, IL-1beta 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-alpha, IL-6, and IL-1beta) 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-alpha, IL-6, and IL-1beta, along with aggravating endotoxin shock-induced markers of organ injury in conscious rats. SN - 1096-0023 UR - https://www.unboundmedicine.com/medline/citation/20004111/Low_dose_erythropoietin_aggravates_endotoxin_induced_organ_damage_in_conscious_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-4666(09)00863-1 DB - PRIME DP - Unbound Medicine ER -