Oztürk O H, Cetin A, Ozdem S S, Uysal N, Kayişli U A, Sentürk U K, Yeşilkaya A
Dept. of Biochemistry, Medical School, Akdeniz Universitesi, Tip Fakültesi, Biyokimya Anabilim Dahli, 07070 Antalya, Turkey.
J Physiol Biochem. 2006 Mar;62(1):27-34. doi: 10.1007/BF03165803.
We investigated the effects of lipopolysaccharide (LPS) administration on plasma nitrite, nitrotyrosine and 6-keto prostaglandin F1alpha, (PGF1alpha) levels and the related resultant changes in function and histochemistry of aorta in rats. Plasma nitrite and PGF1alpha nitrotyrosine levels were analysed after 5 mg/kg intravenous LPS was administered to rats compared with those in non-treated rats. The distribution of nitrotyrosine in the aorta was studied immunohistochemically. The contractile responses of aortic rings to phenylephrine (PE) from both the LPS-treated and control rats were studied in the organ baths. There were increases in plasma nitrite, PGF1alpha, and nitrotyrosine concentrations of LPS-treated rats compared to non-treated rats. Immunoreactivity of nitrotyrosine residues were detected in the endothelial and smooth muscle cells in LPS-treated but not in control rat aorta. The contractile responses to PE of the LPS-treated rat aortic rings were significantly reduced as compared with those of control rat's. Incubation of the aortic rings from LPS-treated rats with cyclooxygenase inhibitor indomethacine or with a combination of indomethacine and nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) increased the contractile responses to the levels observed in control rats suggesting that both prostanoids and particularly nitric oxide (NO) are involved in the reduced contractile responses in LPS-treated rats. These results supported the view that LPS might cause an increment in both NO and PGI2 levels. This increase in the NO and PGI2 levels may be responsible from the reduction in responses of aorta to contractile agents in LPS-treated rats. Increased peroxynitrite formation in LPS-treated rats may lead to nitration of the tyrosil residues of the proteins in the aorta.
我们研究了给予大鼠脂多糖（LPS）对血浆亚硝酸盐、硝基酪氨酸和6-酮前列腺素F1α（PGF1α）水平的影响，以及对大鼠主动脉功能和组织化学的相关影响。将5mg/kg LPS静脉注射给大鼠后，分析其血浆亚硝酸盐、PGF1α和硝基酪氨酸水平，并与未处理大鼠进行比较。采用免疫组织化学方法研究硝基酪氨酸在主动脉中的分布。在器官浴槽中研究LPS处理组和对照组大鼠主动脉环对去氧肾上腺素（PE）的收缩反应。与未处理大鼠相比，LPS处理大鼠的血浆亚硝酸盐、PGF1α和硝基酪氨酸浓度升高。在LPS处理大鼠的主动脉内皮细胞和平滑肌细胞中检测到硝基酪氨酸残基的免疫反应性，而在对照大鼠主动脉中未检测到。与对照大鼠相比，LPS处理大鼠主动脉环对PE的收缩反应明显降低。用环氧化酶抑制剂吲哚美辛或吲哚美辛与一氧化氮合酶抑制剂N（ω）-硝基-L-精氨酸甲酯（L-NAME）联合孵育LPS处理大鼠的主动脉环，可使收缩反应增加至对照大鼠的水平，这表明前列腺素类物质，尤其是一氧化氮（NO）参与了LPS处理大鼠收缩反应的降低。这些结果支持LPS可能导致NO和前列环素I2（PGI2）水平升高的观点。NO和PGI2水平的升高可能是LPS处理大鼠主动脉对收缩剂反应降低的原因。LPS处理大鼠中过氧亚硝酸盐生成增加可能导致主动脉中蛋白质酪氨酸残基的硝化。
