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Regulation of tumor necrosis factor-alpha production in the isolated rat heart stimulated by bacterial lipopolysaccharide or reactive oxygen.
Am Surg. 2004 Sep; 70(9):797-800.AS

Abstract

Reperfusion after cardiopulmonary bypass causes induction of reactive oxygen species (ROS), elevated plasma levels of bacterial lipopolysaccharide (LPS), and production of tumor necrosis factor-alpha (TNF) by the heart. Nuclear factor-kappaB (NF-kappaB) regulates the expression of TNF. Because NF-kappaB is activated by both LPS and ROS, we hypothesized that an inhibitor of NF-kappaB, pyrrolidine dithiocarbamate (PDTC), would block release of TNF from the heart stimulated by these two agents. With Institutional animal care and use committee (IACUC) approval, rat hearts were perfused Langendorf style. LPS was infused and ROS were generated with a hypoxanthine/xanthine oxidase system. PDTC was added to the perfusion buffer. Other hearts were treated with forskolin in order to elevate cyclic AMP. Timed collections of coronary effluent were made for the determination of coronary flow and measurement of TNF. LPS stimulated TNF release to a maximum of 2247 +/- 133 pg/min at 150 minutes. PDTC inhibited LPS-stimulated TNF release. For instance, at 150 minutes, LPS-stimulated TNF release was 449 +/- 49 pg/min with 100 microM PDTC and was 70 +/- 65 pg/mL with 250 microM PDTC (P < 0.05 vs LPS alone). ROS stimulated TNF release was 1494 +/- 130 pg/min at 150 minutes and was not affected by PDTC. Forskolin almost completely blocked TNF release stimulated by LPS or ROS. These data are consistent with the notion that inhibitors of NF-kappaB block cytokine production stimulated by some agents but not others.

Authors+Show Affiliations

Department of Surgery, Mercer University School of Medicine, Macon, Georgia, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15481297

Citation

Jennings, G Russell, et al. "Regulation of Tumor Necrosis Factor-alpha Production in the Isolated Rat Heart Stimulated By Bacterial Lipopolysaccharide or Reactive Oxygen." The American Surgeon, vol. 70, no. 9, 2004, pp. 797-800.
Jennings GR, Castresana MR, Newman WH. Regulation of tumor necrosis factor-alpha production in the isolated rat heart stimulated by bacterial lipopolysaccharide or reactive oxygen. Am Surg. 2004;70(9):797-800.
Jennings, G. R., Castresana, M. R., & Newman, W. H. (2004). Regulation of tumor necrosis factor-alpha production in the isolated rat heart stimulated by bacterial lipopolysaccharide or reactive oxygen. The American Surgeon, 70(9), 797-800.
Jennings GR, Castresana MR, Newman WH. Regulation of Tumor Necrosis Factor-alpha Production in the Isolated Rat Heart Stimulated By Bacterial Lipopolysaccharide or Reactive Oxygen. Am Surg. 2004;70(9):797-800. PubMed PMID: 15481297.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of tumor necrosis factor-alpha production in the isolated rat heart stimulated by bacterial lipopolysaccharide or reactive oxygen. AU - Jennings,G Russell, AU - Castresana,Manuel R, AU - Newman,Walter H, PY - 2004/10/16/pubmed PY - 2004/12/16/medline PY - 2004/10/16/entrez SP - 797 EP - 800 JF - The American surgeon JO - Am Surg VL - 70 IS - 9 N2 - Reperfusion after cardiopulmonary bypass causes induction of reactive oxygen species (ROS), elevated plasma levels of bacterial lipopolysaccharide (LPS), and production of tumor necrosis factor-alpha (TNF) by the heart. Nuclear factor-kappaB (NF-kappaB) regulates the expression of TNF. Because NF-kappaB is activated by both LPS and ROS, we hypothesized that an inhibitor of NF-kappaB, pyrrolidine dithiocarbamate (PDTC), would block release of TNF from the heart stimulated by these two agents. With Institutional animal care and use committee (IACUC) approval, rat hearts were perfused Langendorf style. LPS was infused and ROS were generated with a hypoxanthine/xanthine oxidase system. PDTC was added to the perfusion buffer. Other hearts were treated with forskolin in order to elevate cyclic AMP. Timed collections of coronary effluent were made for the determination of coronary flow and measurement of TNF. LPS stimulated TNF release to a maximum of 2247 +/- 133 pg/min at 150 minutes. PDTC inhibited LPS-stimulated TNF release. For instance, at 150 minutes, LPS-stimulated TNF release was 449 +/- 49 pg/min with 100 microM PDTC and was 70 +/- 65 pg/mL with 250 microM PDTC (P < 0.05 vs LPS alone). ROS stimulated TNF release was 1494 +/- 130 pg/min at 150 minutes and was not affected by PDTC. Forskolin almost completely blocked TNF release stimulated by LPS or ROS. These data are consistent with the notion that inhibitors of NF-kappaB block cytokine production stimulated by some agents but not others. SN - 0003-1348 UR - https://www.unboundmedicine.com/medline/citation/15481297/Regulation_of_tumor_necrosis_factor_alpha_production_in_the_isolated_rat_heart_stimulated_by_bacterial_lipopolysaccharide_or_reactive_oxygen_ L2 - https://www.lens.org/lens/search/patent/list?q=citation_id:15481297 DB - PRIME DP - Unbound Medicine ER -