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Vascular endothelial growth factor and nitric oxide in rat liver regeneration.

机译:血管内皮生长因子和一氧化氮在大鼠肝脏再生中的作用。

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In this work we investigated the role of nitric oxide (NO) in the angiogenesis mediated by vascular endothelial growth factor (VEGF) during rat liver regeneration after two-thirds partial hepatectomy. Sham operated (Sh) and partially hepatectomized (PH) male Wistar rats were randomized in three experimental groups: control (treated with vehicle); pre-treated with sodium nitroprusside (SNP: 0.25 mg/kg body weight, i.v. at a rate of 1 ml/h) and pre-treated with the preferential iNOS inhibitor, aminoguanidine (AG, 100 mg/kg body weight, i.p.). Animals were killed at 5, 24 and 72 h after surgery. At 5 h post-surgery, NO production was estimated by EPR (Sh-Control: 37.65+/-10.70; PH-Control: 88.13+/-1.60(); Sh-SNP: 90.35+/-3.11(); PH-SNP: 119.5+/-12.10()(#); Sh-AG: 33.27+/-5.23, PH-AG: 36.80+/-3.40(#)) (p<0.05 vs Sh-Control; (#)p<0.05 vs PH-Control). At 24 h after PH, VEGF levels showed no difference between PH-Control and PH-SNP animals. However, after 72 h, VEGF protein levels in PH-SNP animals were foundto be increased (above 300%) with respect to PH-Control. On the other hand, aminoguanidine (AG) pre-treatment blocked the rise of inhibition of NO generation and decreased VEGF expression. Our results demonstrated that NO plays a role in modulating VEGF protein expression after hepatectomy in rats.
机译:在这项工作中,我们调查了三分之二的部分肝切除术后大鼠肝脏再生过程中一氧化氮(NO)在由血管内皮生长因子(VEGF)介导的血管生成中的作用。将假手术(Sh)和部分肝切除(PH)的雄性Wistar大鼠随机分为三个实验组:对照组(用赋形剂处理);和对照组。用硝普钠(SNP:0.25 mg / kg体重,静脉内以1 ml / h的速度)预处理,并用iNOS抑制剂氨基胍(AG,100 mg / kg体重,i.p.)预处理。手术后5、24和72小时处死动物。手术后5小时,通过EPR估算未产生NO(Sh-Control:37.65 +/- 10.70; PH-Control:88.13 +/- 1.60(); Sh-SNP:90.35 +/- 3.11(); PH- SNP:119.5 +/- 12.10()(#); Sh-AG:33.27 +/- 5.23,PH-AG:36.80 +/- 3.40(#))(p <0.05 vs Sh-Control;(#)p < 0.05 vs PH-对照)。 PH后24小时,PH对照和PH-SNP动物之间的VEGF水平没有差异。然而,在72小时后,发现PH-SNP动物中的VEGF蛋白水平相对于PH-对照升高(超过300%)。另一方面,氨基胍(AG)预处理阻止了NO产生的抑制作用的上升,并降低了VEGF的表达。我们的结果表明,NO在大鼠肝切除术后可调节VEGF蛋白表达。

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