Signaling pathway of cardioprotection induced by monophosphoryl lipid A in rabbit myocardium.

[1]  M. Favata,et al.  Inhibition of MAP kinase kinase prevents cytokine and prostaglandin E2 production in lipopolysaccharide-stimulated monocytes. , 1998, Journal of immunology.

[2]  R. Thieringer,et al.  Role of stress-activated mitogen-activated protein kinase (p38) in beta 2-integrin-dependent neutrophil adhesion and the adhesion-dependent oxidative burst. , 1998, Journal of immunology.

[3]  S. Kumar,et al.  SB 203580 inhibits p38 mitogen-activated protein kinase, nitric oxide production, and inducible nitric oxide synthase in bovine cartilage-derived chondrocytes. , 1998, Journal of immunology.

[4]  G. T. Elliott Monophosphoryl lipid A induces delayed preconditioning against cardiac ischemia-reperfusion injury. , 1998, Journal of molecular and cellular cardiology.

[5]  A. Harken,et al.  Early and delayed preconditioning: differential mechanisms and additive protection. , 1997, The American journal of physiology.

[6]  P. A. Weber,et al.  Role of inducible nitric oxide synthase in pharmacological "preconditioning" with monophosphoryl lipid A. , 1997, Journal of molecular and cellular cardiology.

[7]  Jiahuai Han,et al.  Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation , 1997, Nature.

[8]  H. Matsuda,et al.  Supplement of nitric oxide attenuates neutrophil-mediated reperfusion injury. , 1995, Circulation.

[9]  Jerry L. Adams,et al.  A protein kinase involved in the regulation of inflammatory cytokine biosynthesis , 1994, Nature.

[10]  M. Currie,et al.  A fluorometric assay for the measurement of nitrite in biological samples. , 1993, Analytical biochemistry.

[11]  D. Latchman,et al.  Cardiac stress protein elevation 24 hours after brief ischemia or heat stress is associated with resistance to myocardial infarction. , 1993, Circulation.

[12]  A. M. Lefer,et al.  The Role of L‐Arginine in Ameliorating Reperfusion Injury After Myocardial Ischemia in the Cat , 1992, Circulation.