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nitric oxide synthase and heme oxygenase expressions in human liver cirrhosis

World Journal of Gastroenterology 2006年第4期12卷 588-594页

作者： Beatrice J Goh Bee Tee Tan Wei Min Hon Kang Hoe Lee Hoon Eng Khoo Department of Biochemistry Yong Loo Lin School of Medicine National University ofSingapore Department of Medicine Yong Loo Lin School of Medicine National University of Singapore Research Biolabs Pte Ltd

AIM： Portal hypertension is a common complication of liver cirrhosis. Intrahepatic pressure can be elevated in several ways. Abnormal architecture affecting the vasculature, an increase in vasoconstrictors and increased circulation from the splanchnic viscera into the portal system may all contribute. It follows that endogenous vasodilators may be able to alleviate the hypertension. We therefore aimed to investigate the levels of endogenous vasodilators, nitric oxide （NO） and carbon monoxide （CO） through the expression of nitric oxide synthase （NOS） and heme oxygenase （HO）. METHOD： Cirrhotic （n = 20） and non-cirrhotic （n = 20） livers were obtained from patients who had undergone surgery. The mRNA and protein expressions of the various isoforms of NOS and HO were examined using competitive PCR, Western Blot and immunohistochemistry. RESULTS： There was no significant change in either inducible NOS （iNOS） or neuronal NOS （nNOS） expressions while endothelial NOS （eNOS） was up- regulated in cirrhotic livers. Concomitantly, caveolin-1, an established down-regulator of eNOS, was upregulated. Inducible HO-1 and constitutive HO-2 were found to show increased expression in cirrhotic livers albeit in different Iocalizations. CONCLUSION： The differences of NOS expression might be due to their differing roles in maintaining liver homeostasis and/or involvement in the pathology of cirrhosis. Sheer stress within the hypertensive liver may induce increased expression of eNOS. In turn, caveolin-1 is also increased. Whether this serves as a defense mechanism against further cirrhosis or is a consequence of cirrhosis, is yet unknown. The elevated expression of HO-1 and HO-2 suggest that CO may compensate in its role as a vasodilator albeit weakly. It is possible that CO and NO have parallel or coordinated functions within the liver and may work antagonistically in the pathophysiology of portal hypertension.

关键词： Liver cirrhosis nitric oxide synthase Heine oxygenase Gene expression Competitive PCR

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nitric oxide synthase AND VASCULAR ENDOTHELIAL GROWTH FACTOR EXPRESSION IN HEPATOCELLULAR CARCINOMA AND THE CORRELATION WITH ANGIOGENESIS

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Chinese Journal of Cancer Research 2001年第2期13卷 124-127页

作者：王鲁汤钊猷孙惠川叶胜龙纪元陆洪芬施达仁 Liver Cancer Institute and Zhongshan Hospital Fudan Medical Center Fudan University Shanghai

Objective: To analyze the expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) in hepatocellular carcinoma (HCC) and its relation to angiogenesis. Methods: Tissue sections from 71 HCC patients were examined immunohistochemically for protein expression of iNOS, eNOS, and VEGF. Microvessal density (MVD) was counted by endothelial cells immunostained by anti-CD34 antibody. Results: Positive immunostaining for iNOS, eNOS was detected in 83.1% and 85.9% of HCC respectively. INOS and eNOS were not detected in normal hepatic tissue. MVD was 34.3±1.5/HP and 38.6±1.6/HP in HCC with positive staining for iNOS and VEGF while it was 31.2±2.8/HP, and 22.4±2.0/HP in HCC with negative staining for iNOS and VEGF (P<0.01). A correlation between NOS expression and VEGF in HCC was not observed. Conclusion: iNOS and eNOS may play a role in malignant transformation f post-hepatic cirrhosis. The expression of iNOS and VEGF favors angiogenesis of HCC.

关键词： Liver carcinoma nitric oxide synthase vascular endothelial growth factor Angiogenesis

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nitric oxide synthase Activity in Arterial Tissues ofCirrhotic Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1997年第1期17卷 25-27页

作者：张丕利梁扩寰林菊生王天才杜荔菁 Institute of Liver Diseases Tongji Hospital Tongji Medical University Wuhan

The changes in the activities of constitutive nitric oxide (NO) synthase (cNOS) and inducible NOS (iNOS) were investigated in arterial tissues of CCl4induced cirrhotic adult SD rats- The aortic tissue homogenate were prepared in normal and cirrhotic rats. NOS activity was measured by conversion of 3H-arginine to H-citrulline. The activities of cNOS and iNOS were calculated in terms of presence or absence of Ca2+. The results showed that activities of total NOS,cNOS and iNOS in arterial tissues were all increased significantly in cirrhotic rats as compared with those in normal controls. There was a significant positive correlation between the activities of total NOS and cGMP content in cirrhotic arterial tissues.

关键词： nitric oxide synthase arterial tissue cirrhosis rats

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Brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase by Ca2+/calmodulin-dependent protein kinase II in rat hippocampus

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Acta Pharmacologica Sinica 2004年第5期25卷 75-80页

作者： Xue-bo YAN, Fan-jie MENG, Bo SONG, Guang-yi ZHANG2Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002, China Research Center for Biochemistry and Molecular Biology Xuzhou Medical College Xuzhou 221002

AIM: To investigate whether brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase(nNOS) by Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the interaction between CaMKIIa and nNOSin rat hippocampus. METHODS: Brain ischemia was induced by bilateral carotid artery occlusion *** and the interaction of proteins were studied by immunoprecipitation and immunoblotting. Weinvestigated during brain ischemia serine phosphorylation and amount of nNOS in crude membranes fraction (P)and cytosolic fraction (S), interaction between CaMKIIa and nNOS, and the effects of 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN-62, a selective inhibitor of CaMKII) on phos-phorylation and the interaction of proteins in P. RESULTS: Serine phosphorylation of nNOS in P increased persis-tently during brain ischemia, and 15 min ischemia-induced serine phosphorylation of nNOS was attenuated signifi-cantly by KN-62. But there was no serine phosphorylation of nNOS in S. The distributions of nNOS were notaffected by ischemia and KN-62. However, the binding levels of both CaMKIIa with nNOS and Thr286autophosphorylated CaMKIIa with nNOS increased after ischemia, and were diminished by KN-62. CONCLUSION:CaMKII interacted with nNOS and regulated serine phosphorylation of nNOS during brain ischemia.

关键词： serine phosphorylation nitric oxide synthase calmodulin kinase KN 62 brain ischemia hippo-campus

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Effect of Dexamethasone on nitric oxide synthase and Caspase-3 Gene Expressions in Endotoxemia in Neonate Rat Brain

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Biomedical and Environmental Sciences 2005年第3期18卷 181-186页

作者： HUAWANG YU-BINWU XIU-HUADU DepartmentofPediatrics SecondClinicalCollegeChinaMedicalUniversityShenyang110004LiaoningChina DepartmentofPediatrics BenxiWomanandChildHospitalBenxi117000LiaoningChina

Objective To investigate the gene and protein expressions of three isoforms of nitric oxide synthase (NOS) and gene expression of Caspase-3, and effect of dexamethasone on them in neonatal rats with lipopolysaccharide (LPS)-induced endotoxemic brain damage. Methods Expressions of the three isoforms of NOS and caspase-3 mRNA in the brain were investigated by RT-PCR in postnatal 7-day wistar rats with acute endotoxemia by intraperitoneal administration of LPS. Regional distributions of NOSs were examined by immunohistochemical technique. Results nNOS and Caspase-3 mRNA were obviously detected. eNOS mRNA was faintly expressed, but iNOS mRNA was undetectable in the control rat brain. The expressions of NOS mRNA of three isoforms were weak 2 h after LPS (5 mg/mg) delivery, peaked at 6 h, and thereafter, reduced gradually up to 24 h. The expression intensity was in the order of nNOS> iNOS> eNOS. Widespread nNOS, scattered eNOS distribution and negative iNOS were identified in the control rat brain and all isoforms of NOS could be induced by LPS which reached the apex at 24 h in the order of nNOS> iNOS> eNOS as detected by immunostaining. Although Caspase-3 mRNA could be found in all groups, DNA fragmentation was only seen at 6 h and 24 h. The expressions of NOS and Caspase-3 mRNA were inhibited in the rat brain when dexamethasone was administrated. Conclusion LPS-induced NO production induces apoptosis of neurons through mechanism involving the Caspase-3 activation, which may play an important role in the pathogenesis of brain damage during endotoxemia, and neuro-protective effects of dexamethasone may be partially realized by inhibiting the expression of NOS mRNA.

关键词： Lipopolysaccharide Endotoxemia Brain nitric oxide synthase Caspase-3

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Inducible nitric oxide synthase expression is related to angiogenesis,bcl—2 and cell proliferation in hepatocellular carcinoma

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Journal of Zhejiang University Science 2003年第2期4卷 221-227页

作者：彭佳萍郑树孝作祥张苏展 CancerInstitute CollegeofMedicineZhejiangUniversityHangzhou310009China

In this study, we examined the expression of inducible nitric oxide s ynthase (iNOS) and vascular endothelial growth factor (VEGF) by immunohistoc hemi cal staining in 76 tissue sections collected from hepatocellular carcinoma (HCC) patients undergoing hepatectomy. Microvascular density (MVD) was determined by counting endothelial cells immunostained using anti-CD34 antibody. We performe d DNA-flow cytometric analyses to elucidate the impact of iNOS and VEGF expressi o n on the cell cycle of HCC. Most of the HCC cells that invaded stroma were mark edly immunostained by iNOS antibody. The iNOS stain intensity of the liver tissu e close to the tumor edge was stronger than that of HCC tissue, and the stronges t was the hepatocytes closer to the tumor tissue. However, iNOS expression in 10 normal hepatic samples was undetectable. VEGF positive expression ratio was 84. 8% in iNOS positive expression cases, and the ratio was 35.3% in negative cases. There was significant correlation (P=0.000) between iNOS and VEGF expressi on. Moreover, iNOS expression was significantly associated with bcl-2 and MVD, but w ithout p53 expression. DNA-flow cytometric analyses showed that combined expres s ion of iNOS and VEGF had significant impact on the cell cycle in HCC. PI (Proli ferating Index) and SPF (S-phase fraction) in the combined positive expression o f iNOS and VEGF group was significantly higher than that in the combined negativ e group. The present findings suggested that iNOS expression was significantly a ssociated with angiogenesis, bcl-2 and cell proliferation of HCC.

关键词： Hepatocellular carcinoma nitric oxide synthase Angiog enesis Bcl-2 Flow cytometric analyse

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Rosuvastatin reduces rat intestinal ischemia-reperfusion injury associated with the preservation of endothelial nitric oxide synthase protein

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World Journal of Gastroenterology 2006年第13期12卷 2024-2030页

作者： Yuji Naito Kazuhiro Katada Tomohisa Takagi Hisato Tsuboi Masaaki Kuroda Osamu Handa Satoshi Kokura Norimasa Yoshida Hiroshi Ichikawa Toshikazu Yoshikawa Department of Medical Proteomics Kyoto Prefectural University of Medicine Kyoto 602-8566Japan Inflammation and Immunology Graduate School of Medical Science Kyoto Prefectural University of MedicineKyoto 602-8566Japan Department of Biomedical Safety Science Kyoto Prefectural University of Medicine Kyoto 602-8566Japan Molecular Gastroenterology and Hepatology Graduate School of Medical Science Kyoto Prefectural University of MedicineKyoto 602-8566Japan Department of Food Sciences and Nutritional Health The Faculty of Human Environment Kyoto Prefectural UniversityKyoto 606-8522Japan

AIM： To investigate the protective effect of rosuvastatin on ischemia-reperfusion （I-R）-induced small intestinal injury and inflammation in rats, and to determine the effect of this agent on the expression of endothelial nitric oxide synthase （eNOS） protein. METHODS： Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion for 60 min. Rosuvastatin dissolved in physiological saline was administered intraperitoneally 60 min before ischemia. The severity of the intestinal mucosal injury and inflammation were evaluated by several biochemical markers, as well as by histological findings. The protein levels of eNOS were determined by Western blot. RESULTS： The levels of both intraluminal hemoglobin and protein, as indices of mucosal damage, were significantly increased in the I-R group compared with those in the sham-operated group. These increases, however, were significantly inhibited by treatment with rosuvastatin in a dose-dependent manner. The protective effects of rosuvastatin were also confirmed by histological findings. Exposure of the small intestine to I-R resulted in mucosal inflammation characterized by significant increases in thiobarbituric acid-reactive substances, tissueassociated myeloperoxidase activity, and the mucosal contents of rat cytokine-induced neutrophil chemoattracrant-1 （CINC-1） and tumor necrosis factor-α（TNF-α）. These increases in inflammatory parameters after I-R were significantly inhibited by pretreatment with rosuvo astatin at a dose of 10 mg/kg. Furthermore, mRNA expression of CINC-1 and TNF-α was increased after I-R, and this increase was also inhibited by rosuvastatin. The mucosal protein levels of eNOS decreased during I-R, but were preserved in rats treated with rosuvastatin. CONCLUSION： Rosuvastatin inhibits rat intestinal injury and inflammation induced by I-R, and its protection is associated with the preservation of eNOS pro

关键词： Rosuvastatin Rat Intestine Ischemia-reperfusion injury Endothelium nitric oxide synthase

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Effects of icariin on erectile function and expression of nitric oxide synthase isoforms in castrated rats

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Asian Journal of Andrology 2005年第4期7卷 381-388,页

作者： Wu-Jiang Liu Zhong-Cheng Xin Hua Xin Yi-Ming Yuan Long Tian Ying-Lu Guo Andrology Center of Peking University First Hospital Beijing 100009 China

Aim： To investigate the effect of icariin on erectile function and the expression of nitric oxide synthase （NOS） isoforms in castrated rats. Methods： Thirty-two adult male Wistar rats were randomly divided into one shamoperated group （A） and three castrated groups （B, C and D）. One week after surgery, rats were treated with normal saline （groups A and B） or oral icariin （1 mg/[kg·day] for group C and 5 mg/[kg·day] for group D） for 4 weeks. One week after treatment, the erectile function of the rats was assessed by measuring intracavernosal pressure （ICP） during electrostimulation of the cavernosal nerve. The serum testosterone （ST） levels, the percent of smooth muscle （PSM） in trabecular tissue, and the expression of mRNA and proteins of neuronal nitric oxide synthase （nNOS）, inducible nitric oxide synthase （iNOS）, endothelial nitric oxide synthase （eNOS） and phosphodiesterase V （PDES） in corpus cavernosum （CC） were also evaluated. Results： ICP, PSM, ST and the expression of nNOS, iNOS, eNOS and PDE5 were significantly decreased in group B compared with those in group A （P 〈 0.01）. However, ICE PSM and the expression of nNOS and iNOS were increased in groups C and D compared with those in group B （P 〈 0.05）. Changes in ST and the expression of eNOS and PDE5 were not significant （P 〉 0.05） in groups C and D compared with those in group B. Conclusion： Oral treatment with icariin （〉 98.6 % purity） for 4 weeks potentially improves erectile function. This effect is correlated with an increase in PSM and the expression of certain NOS in the CC of castrated rats. These results suggest that icariin may have a therapeutic effect on erectile dysfunction.

关键词： icariin corpus cavernosm intracavernosal pressure nitric oxide synthase erectile dysfunction

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Effect of verapamil on nitric oxide synthase in a portal veinligated rat model: Role of prostaglandin

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World Journal of Gastroenterology 2006年第15期12卷 2351-2356页

作者： Chii-Shyan Lay CMY May Fa-Yauh Lee Yang-Te Tsai Shou-Dong Lee Shu Chien Shiomoh Sinchon Division of Hepatology and Gastroenterology Department of Internal Medicine China Medical University HospitalTaichungChina Division of Gastroenterology Department of Internal Medicine Veterans General HospitalTaipeiNational Yang-Ming University School of MedicineTaipeiChina Institute of Biomedical Sciences Academia Sinica TaiwanChina Department of Medicine Columbia University New York University Medical CenterNew YorkUSA

AIM： To investigate the effects of verapamil on nitric oxide （NO） synthesis in a portal vein-ligated rat model. METHODS： Systemic and splanchnic hemodynamics were measured by radiolabeled microspheres in portal hypertensive rats after acute administration of verapamil （2 mg/kg） on chronic treatment with N^W-nitro-L-arginine （NNA）（80 mg/kg） and/or indomethacin （2 mg/kg） . RESULTS： Verapamil （2 mg/kg） caused a marked fall in both arterial pressure and cardiac output accompanied by an insignificant change in the portal pressure and no change in portal venous inflow. This result suggested that verapamil did not cause a reduction in portal vascular resistance of portal hypertensive rats, which was similar between N^w- nitro-Loarginine-treated and indomethacin-treated groups. CONCLUSION： In portal hypertensive rats pretreated with NNA and/or indomethacin, acute verapamil administration can not reduce the portal pressure, suggesting that NO and prostaglandin play an important role in the pathogenesis of splanchnic arterial vasodilation in portal hypertension.

关键词： Verapamil nitric oxide synthase Portal hypertension

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Agmatine reduces nitric oxide synthase expression and peroxynitrite formation in the cerebral cortex in a rat model of transient global cerebral ischemia

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Neural Regeneration Research 2010年第23期5卷 1773-1781页

作者： Chin Hee Mun Won Taek Lee Kyung Ah Park Jong Eun Lee Department of Anatomy Yonsei University College of Medicine Brain Korea 21 Project for Medical Science Yonsei University College of Medicine

Agmatine, an analog of L-arginine, is an endogenous substance synthesized by arginine decarboxylase, which has been shown to possess neuroprotective effects following brain ischemia. nitric oxide is generated by sequential oxidation of the guanidinium group in L-arginine, and agmatine might protect the brain from ischemic injury by interfering with nitric oxide signaling. This study investigated the effects of agmatine on cerebral cortex neuronal injury following transient global cerebral ischemia and also detected nitric oxide synthase expression and peroxynitrite formation. Results demonstrated that intraperitoneal injection of agmatine in global cerebral ischemia/reperfusion alleviated ischemia/reperfusion-induced cerebral cortical cortex neuronal injury and cellular apoptosis, decreased neuronal and inducible nitric oxide synthase expression at 24, 48, and 72 hours following global cerebral ischemia and reperfusion, and greatly inhibited nitrotyrosine levels, which reflect the amount of peroxynitrite formed. These findings indicated that agmatine alleviates cerebral cortex neuronal injury following global cerebral ischemia and decreases nitric oxide synthase expression and peroxynitrite formation following ischemia/repeffusion.

关键词： agmatine global cerebral ischemia cerebral cortex nitric oxide nitric oxide synthase neuroprotection

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