Mechanism of the production of reactive nitrogen species during renal ischemic-reperfusion insult
Mechanism of the production of reactive nitrogen species during renal ischemic-reperfusion insult
批准号:
13670087
负责人:
TAMAKI Toshiaki
金额:
$2.24万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2002
中文摘要
在循环中,一氧化氮(NO)以相对稳定的血红蛋白-NO加合物(HbNO)形式存在,这意味着HbNO的量可以反映血液中NO的浓度。已报道使用电子顺磁共振(EPR)方法成功地在人血液中检测到HbNO信号。然而,有一些困难,以获得良好的HbNO信号的正常血液。为了克服这一困难,我们引入了EPR信号相减法。用此方法,我们证实了L-精氨酸可增加戊巴比妥麻醉大鼠的HbNO浓度,而D-精氨酸则无此作用。血管紧张素转换酶(ACE)抑制剂替莫普利(Temocapril)可改善L-MAME诱导的高血压大鼠的NO动力学异常<15>。左肾开放后5分钟,取左、右肾组织及静脉血。用<15>EPR法测定肾组织及静脉血Hb、NO浓度。左<15>肾(缺血)组织Hb、NO浓度明显高于右肾(非缺血)组织。缺血<15>再灌注大鼠静脉血Hb、NO浓度明显高于非缺血组。结果表明,缺血再灌注损伤可促进NO_2生成NO
英文摘要
In circulation, nitric oxide(NO) exists as relatively atable hemoglobin-NO adduct(HbNO), which means that the amount of HbNO may reflect the blood NO concentration. HbNO signal has been reported to be successfully detected in human blood using electron paramagnetic resonance(EPR) method. However, there were some difficulties to obtain a fine HbNO signal of nornal blood. We itroduced the EPR signal subtraction method to overcome the difficulties. Using this method, we confirmed that HbNO concentrarion in pentobarbital-anesthetized rats were augmented by infusion of L-arginine but not D-argimine. We also emenstrated that temocapril, an ACE inhibitor, improved abnormalities of NO dynamics in the L-MAME-induced hypertensive rats.After the intravebous infusion of ^<15>NO_2, the left renal artery of a rat was clumped for 40 minutes. Five minutes after the release of left renal occluaion, left and right renal tissues and venous blood were obtained. Hb^<15>NO concentration of renal tissues and venous blood was evaluated using EPR method. Hb^<15>NO concentrarion of left (ischemic) renal tissue is much higher than that of right(non-ischemic) renal tissue. Hb^<15>NO concentration of venous blood in ischemic-reperfused rat is much higher than that in aham operated non-ischemic rat. These results indicate that there is NO generation pathway from NO_2 and ischemic-reperfusion insult stimulates the NO generation from NO_2
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K.Tsuchiya: "The role of thiol and nitrosothiol compounds in the nitric oxide-forming reactions of the iron-N-methyl-D-glucamine dithiocarbamate complex"Biochemical Journal. 367. 771-779 (2002)
K.Tsuchiya:“硫醇和亚硝基硫醇化合物在铁-N-甲基-D-葡萄糖胺二硫代氨基甲酸盐复合物的一氧化氮形成反应中的作用”生物化学杂志。
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土屋浩一郎: "亜硝酸と一酸化窒素(NO)"血管. 25. 63-71 (2002)
土屋晃一郎:“亚硝酸盐和一氧化氮 (NO)”血管。25. 63-71 (2002)
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S.Kagami: "Requirement for tyrosine kinase-ERK1/2 signaling in α1β1 integrin-mediated collagen matrix remodeling by rat mesangial cells"Experimental Cell Research. 268. 274-283 (2001)
S. Kagami:“大鼠系膜细胞 α1β1 整合素介导的胶原基质重塑中酪氨酸激酶-ERK1/2 信号传导的要求”实验细胞研究 268. 274-283 (2001)。
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M.Yoshizumi, T.Kogane, Y.Suzaki, K.Kirima, Moe Kyaw, K.Kirima, K.Ishizawa, K.Tsuchiya, S.Kagami, T.Tamaki: "Ebeelen attenuates oxidative styress-induced apoptosis via the inhibition of the c jun N-terminal kinase and activator protein-1 signaling pathway
M.Yoshizumi、T.Kogane、Y.Suzaki、K.Kirima、Moe Kyaw、K.Kirima、K.Ishizawa、K.Tsuchiya、S.Kagami、T.Tamaki:“Ebeelen 通过抑制来减弱氧化苯乙烯诱导的细胞凋亡
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K.Tsuchiya, K.Kirima, M.Yoshizumi, H.Houchi, T.Tamaki, RP.Mason: "The role of thiol and nitrosothiol compounds in the nitric oxide-forming reactions of the iron-N-methyl-D-glucamine dithiocarbamate complex"Biochemical Journal. 367. 771-779 (2002)
K.Tsuchiya、K.Kirima、M.Yoshizumi、H.Houchi、T.Tamaki、RP.Mason:“硫醇和亚硝基硫醇化合物在铁-N-甲基-D-葡萄糖胺的一氧化氮形成反应中的作用
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共 21 条
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