title: Interaction between endogenous nitric oxide and carbon monoxide in the pathogenesis of recurrent febrile seizures.
abstract: The aim of the study was to investigate the interaction between nitric oxygenase (NOS)/nitric oxide (NO) and heme oxygenase (HO)/carbon monoxide (CO) system in the pathogenesis of recurrent febrile seizures (FS). On a rat model of recurrent FS, the ultrastructure of hippocampal neurons was observed under electron microscopy, and expression of neuronal NOS (nNOS) in hippocampus and NO formation in plasma were examined after treatment with ZnPP-IX, an HO-1 inhibitor. In the ultrastructure of hippocampal neurons, the expression of HO-1 in hippocampus and CO formation in plasma were examined after treatment with L-NAME, a NOS inhibitor. We found that hippocampal neurons were injured after recurrent FS. The gene and protein expression of nNOS and HO-1 increased markedly in hippocampus in FS rats, while CO formation in plasma increased markedly and the concentration of NO in plasma increased slightly. ZnPP-IX could worsen the neuronal damage of recurrent FS rats. However, it further increased the expression of nNOS and endogenous production of NO obviously. L-NAME alleviated the neuronal damage of recurrent FS rats, but decreased the expression of HO-1 and CO formation. The results of this study suggested that endogenous NOS/NO and HO/CO systems might interact with each other and therefore play an important regulating role in recurrent FS brain damage.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, People's Republic of China. zhixian.yang@163.com
authors.forename: Zhi-Xian
authors.initials: ZX
authors.lastname: Yang
authors.forename: Jiong
authors.initials: J
authors.lastname: Qin
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology; D002248:Carbon Monoxide / Q000378:metabolism*; D002951:Citrates / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism; D004195:Disease Models, Animal; D004587:Electrophoresis, Agar Gel; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004996:Ethidium / Q000494:pharmacology; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D006624:Hippocampus / Q000648:ultrastructure; D007150:Immunohistochemistry; D007364:Intercalating Agents / Q000494:pharmacology; D007854:Lead / Q000494:pharmacology; D008297:Male; D008854:Microscopy, Electron; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D009942:Organometallic Compounds / Q000494:pharmacology; D010088:Oxidoreductases / Q000378:metabolism; D011524:Protoporphyrins / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012008:Recurrence; D020133:Reverse Transcriptase Polymerase Chain Reaction; D003294:Seizures, Febrile / Q000209:etiology* / Q000473:pathology
chemical_list: D002951:Citrates; D004791:Enzyme Inhibitors; D007364:Intercalating Agents; D009942:Organometallic Compounds; D011524:Protoporphyrins; C017803:zinc protoporphyrin; C005460:uranyl acetate; D007854:Lead; D009569:Nitric Oxide; D002248:Carbon Monoxide; D010088:Oxidoreductases; D006419:Heme Oxygenase (Decyclizing); C034747:nitric-oxide reductase; D004996:Ethidium; D006152:Cyclic GMP; D019331:NG-Nitroarginine Methyl Ester