Influence of L-arginine on the Expression of eNOS and COX2 in Experimental Pulmonary Thromboembolism

The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatme...

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Published inJournal of Huazhong University of Science and Technology. Medical sciences Vol. 26; no. 5; pp. 524 - 527
Main Author 张建初 夏蕾 张晓菊 杨卫兵 白明
Format Journal Article
LanguageEnglish
Published China Department of Pulmonary Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan 430022, China%Department of Pulmonary Medicine, Affiliated Hospital of Wuhan University of Science & Technology, Wuhan 430064, China 2006
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ISSN1672-0733
1993-1352
DOI10.1007/s11596-006-0509-4

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Abstract The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGF1 α were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P〈0.01), and the levels of TXB2, 6-Keto-PGF1α and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P〈0.05), while that of COX2 protein and mRNA was upregulated (P〈0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1 α was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P〈0.05), while that of COX2 protein and mRNA was down-regulated (P〈0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.
AbstractList The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGFla were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P<0.01), and the levels of TXB2, 6-Keto-PGF1alpha and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P<0.05), while that of COX2 protein and mRNA was upregulated (P<0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1alpha was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P<0.05), while that of COX2 protein and mRNA was down-regulated (P<0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGFla were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P<0.01), and the levels of TXB2, 6-Keto-PGF1alpha and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P<0.05), while that of COX2 protein and mRNA was upregulated (P<0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1alpha was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P<0.05), while that of COX2 protein and mRNA was down-regulated (P<0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.
R3; The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism.Plasma NO, TXB2 and 6-Keto-PGF1α were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively.The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P<0.01), and the levels of TXB2,6-Keto-PGF1α and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P<0.05), while that of COX2 protein and mRNA was upregulated (P<0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1 α was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P<0.05), while that of COX2 protein and mRNA was down-regulated (P<0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.
The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGFla were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P<0.01), and the levels of TXB2, 6-Keto-PGF1alpha and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P<0.05), while that of COX2 protein and mRNA was upregulated (P<0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1alpha was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P<0.05), while that of COX2 protein and mRNA was down-regulated (P<0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.
The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGF1 α were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P〈0.01), and the levels of TXB2, 6-Keto-PGF1α and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P〈0.05), while that of COX2 protein and mRNA was upregulated (P〈0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1 α was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P〈0.05), while that of COX2 protein and mRNA was down-regulated (P〈0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.
Author 张建初 夏蕾 张晓菊 杨卫兵 白明
AuthorAffiliation Department of Pulmonary Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China Department of Pulmonary Medicine, Affiliated Hospital of Wuhan University of Science & Technology, Wuhan 430064, China
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10.1161/01.ATV.15.2.258
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pulmonary thromboembolism
nitric oxide synthase
L-arginine
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nitric oxide synthase
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T. W. Wakefield (509_CR3) 1995; 15
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Snippet The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism...
The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and...
R3; The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism...
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SubjectTerms Animals
Arginine - pharmacology
Arginine - therapeutic use
Cyclooxygenase 2 - genetics
Cyclooxygenase 2 - metabolism
Female
L-精氨酸
Lung - enzymology
Male
Nitric Oxide Synthase Type III - genetics
Nitric Oxide Synthase Type III - metabolism
Pulmonary Embolism - drug therapy
Pulmonary Embolism - enzymology
Rats
Rats, Wistar
RNA, Messenger - genetics
RNA, Messenger - metabolism
基因表达
肺血管栓塞
Title Influence of L-arginine on the Expression of eNOS and COX2 in Experimental Pulmonary Thromboembolism
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