A COX/5-LOX Inhibitor Licofelone Revealed Anticonvulsant Properties Through iNOS Diminution in Mice
Borna PayandemehrMahsima KhoshneviszadehBardia VarastehmoradiRamtin GholizadehTaraneh BahremandHossein AttarArash BahremandAhmad Reza Dehpour
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The activity of inducible nitric oxide synthase(iNOS) in the liver,the concentration of nitric oxide(NO) in the serum,the coccidian oosysts per gram feces(OPG)and anatomic structures of rabiits' livers and micoscopic pathological changes were studied.The rabbits infected with Eimeria stiedai were injected with the substrate of nitric oxide synthase—L-arginine(L-Arg) with different concentrations and the inhibitor of inducible nitric oxide synthase-L-aminoguanidine(L-AG) through the abdominal cavity.The results showed that after infected with Eimeria stiedai,the activity of inducible nitric oxide synthase of rabbits' liver chips and the concentration of nitric oxide in the serum increased gradually.The control group,L-arginine group,and L-aminoguanidine group reached the top after infected 12 days,and then decreased gradually and reached the level before infected at about 23days;L-arginine could enhance the activity of inducible nitric oxide synthase in the liver and make it release large amount of nitric oxide,inhibit or kill Eimeria stiedai and ease the pathologies caused by Eimeria stiedai;On the contrary,L-aminoguanidine inhibits inducible nitric oxide synthase in the liver and reduces nitric oxide produced,so that the inhibition on Eimeria stiedai was weakened or even not existed andaggravated the pathologies.The results implied that nitric oxide and inducible nitric oxide synthase indeed participate in the process of rabbits' infection with Eimeria stiedai and nitric oxide played the definite role of inhibition or killness on coccidia of rabbites.
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This study is to explore the effects of extracts of Cheezheng pain relieving plaster (ECPRP) on nitric oxide (NO) production and expression of inducible nitric oxide synthase (iNOS) in macrophages induced by LPS and the mechanism involved. Nitric oxide level was measured with Griess reagent assay. Inducible nitric oxide synthase (iNOS) protein and NF-kappaBp65 fragment were detected with Western blotting. ECPRP (62.5 and 125 mgL(-1)) significantly inhibited the increase of nitric oxide level. Furthermore, ECPRP (62.5 and 125 mg x L(-1)) notably reduced the expression of iNOS mRNA and protein. ECPRP (62.5 and 125 mg x L(-1)) elevated the content of I-kappaB protein in cytoplasm, while decreased the content of NF-kappaBp65 protein in nucleus. These results suggest that ECPRP reduce nitric oxide level via down-regulation of NF-kappaB-iNOS-nitric oxide pathway, resulting in prevention of inflammation.
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To probe into the activity of inducible nitric oxide synthase(iNOS) in the liver,the concentration of nitric oxide(NO) in the serum and its inhibition or killness on coccidia of rabbits,the rabbits infected with Eimeria stiedai were injected with the substrate of nitric oxide synthase-L-arginine(L-Arg) with different concentrations,the nitric oxide donor-nitroglycerin(GTN) and the inhibitor of inducible nitric oxide synthase-L-aminoguanidine(L-AG) through the abdominal cavity.Then messure the activity of inducible nitric oxide synthase in the liver using test box of nitric oxide synthase activity.Messure the concentration of nitric oxide in the serum via the method of nitric acid reductase.Count the coccidian oosysts per gram feces(OPG) using McMaster's method.Score the pathologies according to anatomic structures of rabiits' livers and micoscopic pathological changes.The results showed that: after infected with Eimeria stiedai,the activity of inducible nitric oxide synthase of rabbits' liver chips and the concentration of nitric oxide in the serum increased gradually.The control group,L-arginine group,nitroglycerin group and L-aminoguanidine group reached the top 12 days after infected,and then decreased gradually and reached the level before infected at about 23days;L-arginine can enhance the activity of inducible nitric oxide synthase in the liver and make it release large amount of nitric oxide,so that inhibit or kill Eimeria stiedai and ease the pathologies caused by Eimeria stiedai;Nitroglycerin can release nitric oxide in vivo and inhibit Eimeria stiedai,so that ease the pathologies.On the contrary,L-aminoguanidine inhibits inducible nitric oxide synthase in the liver and reduces nitric oxide produced,so that the inhibition on Eimeria stiedai was weakened or even not existed andaggravated the pathologies.The results clues on that nitric oxide and inducible nitric oxide synthase indeed participate in the process of rabbits' infection with Eimeria stiedai and nitric oxide plays the role of inhibition or killing in the process of infection.
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The role of nitric oxide in the immune response to allogeneic tissue was explored in an in vivo cardiac transplant model in the rat. Nitric oxide production during organ rejection was demonstrated by elevations in systemic serum nitrite/nitrate levels and by electron paramagnetic resonance spectroscopy. Messenger RNA for the inducible nitric oxide synthase enzyme was detected in the rejecting allografted heart, but not in the nonrejecting isografted heart. The enzyme was demonstrated to be biologically active by the in vitro conversion of L-arginine to L-citrulline and was immunohistochemically localized to the infiltrating inflammatory cells. Treatment with aminoguanidine, a preferential inhibitor of the inducible nitric oxide synthase isoform, prevented the increased nitric oxide production in the transplanted organ and significantly attenuated the pathogenesis of acute rejection. Aminoguanidine treatment prolonged graft survival, improved graft contractile function, and significantly reduced the histologic grade of rejection. These results suggest an important role for nitric oxide in mediating the immune response to allogeneic tissue. Inhibition of inducible nitric oxide synthase may provide a novel therapeutic modality in the management of acute transplant rejection and of other immune-mediated processes.
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Inflammation is a process consisting of a complex of cytological and chemical reactions which occur in and around affected blood vessels and adjacent tissues in response to an injury caused by a physical, chemical or biological insult. Much work has been performed in the past several years investigating inducible nitric oxide synthase (NOS, EC 1.14.13.39) and nitric oxide in inflammation. This has resulted in a rapid increase in knowledge about iNOS and nitric oxide. Nitric oxide formation from inducible NOS is regulated by numerous inflammatory mediators, often with contradictory effects, depending upon the type and duration of the inflammatory insult. Equine medicine appears to have benefited the most from the increased interest in this small, inflammatory mediator. Most of the information on nitric oxide in traditional veterinary species has been produced using models or naturally occurring inflammatory diseases of this species.
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Nitric oxide (NO), a gas signal molecule, is produced by nitric oxide synthase (NOS) and has many physiological functions. Inducible NOS (iNOS) and NO not only promote or inhibit tumors, but also have many applications in cancer treatment. This article reviews the role and treatment of iNOS and NO in tumors.
Key words:
Neoplasms; Nitric oxide synthase; Nitric oxide
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