Animals ; Blood Platelets ; cytology ; Bone Marrow Cells ; cytology ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Cyclophosphamide ; Female ; Fibroblasts ; cytology ; Male ; Megakaryocytes ; cytology ; Mice ; Stem Cells ; cytology ; Thrombocytopenia ; chemically induced ; therapy

AIMTo determine the protective effect and influence on NOS expression of Montelukast sodium--a leukotriene antagonist on myocardial necrosis in rats.

METHODSMyocardial ischemia and necrosis were induced in rats by isoproterenol (2 mg.kg-1, s.c., qd for 2 d). Serum activity of LDH, CK, MDA, NO content in myocardium and scope of myocardial necrosis were measured. nNOS, iNOS and eNOS were investigated by immunohistochemical evaluation.

RESULTSDecreased serum level of LDH, CK, MDA and attenuated myocardial necrosis area were found in rats pretreated with Montelukast sodium 10 and 30 mg.kg-1. Montelukast sodium 30 mg.kg-1 also enhanced NO content in myocardium. Montelukast sodium activated the eNOS expression and reduced the iNOS expression.

CONCLUSIONMontelukast sodium is cardioprotective during myocardial injury in rats by halting the leukotrienes-induced inflammatory response and upregulating the eNOS expression as well as downregulating the iNOS expression. This may represent an approach to the treatment of myocardial ischemia with leukotriene antagonists.

Acetates ; pharmacology ; Animals ; Cardiotonic Agents ; pharmacology ; Female ; Isoproterenol ; Leukotriene Antagonists ; pharmacology ; Male ; Myocardial Ischemia ; chemically induced ; enzymology ; pathology ; Myocardium ; metabolism ; pathology ; Necrosis ; Nitric Oxide Synthase ; metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Quinolines ; pharmacology ; Rats ; Rats, Sprague-Dawley

To investigate the changes of platelet activated state and platelet activated function by trace whole blood flow cytometry (FCM), and to explore the mechanism of hemorrhage and infiltration in adults with acute leukemia, the expression percentage and changes of these expressions of CD62p and PAC-1 on platelet surface were determined by FCM of trace whole blood after platelet activated by ADP in patients with new diagnosed AL (group I), complete remission (CR, group II) and continuously complete remission (CCR, group III). Healthy adults were used as control group. The result showed that the expression of CD62p in group I and II was higher than that in control group, before and after platelet activated by ADP (P < 0.01). The expression of PAC-1 in group I was higher than that in control group (P < 0.01), the expression of PAC-1 in group II was lower than that in control group (P > 0.01), There was no significant difference in expression of CD62p and PAC-1 between group III and control group (P > 0.01), and no significant difference was found between AL group with megakaryocyte malignant pathological changes and AL group without megakaryocyte malignant pathological changes before platelet activated by ADP (P > 0.01). After platelet activated by ADP, the expression of PAC-1 in the former was lower than that in the latter (P < 0.01). It is concluded that (1) high level activated platelet in peripheral blood of AL patients show that interaction between activated platelet and leukemia cells can be one of reason resulting in widespread hemorrhage and infiltration AL patiens; (2) the decrease of number and activted function of platelet at the first stage of AL patients may be caused by malignant hyperplasia of leukemia cells and damage of megakaryopoiesis in bone marrow.
Acute Disease ; Adenosine Diphosphate ; pharmacology ; Adolescent ; Adult ; Aged ; Blood Platelets ; cytology ; metabolism ; Cell Membrane ; drug effects ; metabolism ; Female ; Flow Cytometry ; Humans ; Leukemia ; blood ; pathology ; Male ; Middle Aged ; P-Selectin ; biosynthesis ; Platelet Activation ; drug effects ; physiology ; Platelet Glycoprotein GPIIb-IIIa Complex ; biosynthesis

Adult ; Animals ; Female ; Frameshift Mutation/genetics* ; Genes, sry ; Gonadal Dysgenesis, 46,XY/genetics* ; Humans ; Menarche ; Ovary/pathology* ; Oviducts/pathology* ; Sex-Determining Region Y Protein/genetics*