氧化应激相关酶及信号通路蛋白表达对动静脉内瘘患者血栓形成的影响

Influence of oxidative stress-related enzymes and signal pathway protein expression on thrombosis in patients with arteriovenous fistula

摘要:

目的  探讨氧化应激相关酶及信号通路蛋白表达对动静脉内瘘（AVF）患者血栓形成的影响。 方法  该院血液中心于2014年1月-2016年1月收治120例行AVF手术或AVF修补术的肾脏疾病患者依据AVF术后是否有血栓形成分为两组：A组71例（AVF术后有血栓形成），B组49例（AVF术后无血栓形成），比较两组患者氧化应激酶及信号通路蛋白水平。结果  A组血浆甲状旁腺激素、半胱氨酸水平高于B组（P =0.000和0.000），血红蛋白、C反应蛋白水平低于B组，差异有统计学意义（P =0.000和0.000）；A组患者血管组织中超氧化物歧化酶-1（SOD-1）、超氧化物歧化酶-2（SOD-2）、血红素氧化酶-1（HO-1）、Ras相关C3肉毒素酶解-2（Rac-2）和还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶（NOX-4）水平高于B组，差异有统计学意义（P =0.000、0.000、0.000、0.000和0.000）；A组患者血管组织中NADPH氧化酶亚单位P-22、磷脂酰肌醇3激酶（PI3K）、叉头框蛋白01（P-Fox01）和叉头框蛋白03a（P-Fox03a）水平高于B组，差异有统计学意义（P =0.000、0.000、0.000和0.000）；内瘘患者血栓形成与血管组织中SOD-1、SOD-2、HO-1、Rac-2、NOX-4、P-22、P13K、P-Fox01和P-Fox03a水平呈正相关（P =0.040、0.010、0.041、0.022、0.030、0.021、0.031、0.020和0.021）。 结论  氧化应激反应通过P13K/Fox0信号通路传导表达相关酶及蛋白，引发血管内皮损伤，导致动静脉内瘘吻合处狭窄及血栓形成，临床可通过干预动静脉内瘘患者体内应激反应及相关信号通路蛋白表达预防或治疗动静脉内瘘血栓的形成。

Abstract:

Objective To investigate the influence of oxidative stress-related enzymes and signal pathway protein expression on arteriovenous fistula (AVF) in patients with thrombosis. Methods From January 2014 to January 2016, 120 patients treated with routine arteriovenous fistula (AVF) or AVF repair surgery were divided into two groups according  whether AVF thrombosis occurred after surgery: A group of 71 cases (AVF thrombosis after surgery), group B had 49 cases(AVF postoperative thrombosis). Levels of blood biochemical marker, oxidative stress-related enzymes (SOD-1, SOD-2, HO-1, Rac- 2 and NOX-4) and related signaling pathway proteins (P-22, P13K, P-Fox01 and P-Fox03a) were compared. Results Levels ofplasma parathyroid hormone, homocysteine in group Awere significantly higher than group B (P = 0.000, 0.000), and hemoglobin, C-reactive protein levels were significantly lower than group B, the differences were significant (P = 0.000, 0.000). Levels of SOD-1, SOD-2, HO-1, Rac-2 and NOX-4 in group A were significantly higher than group B, the differences were statistically significant (P = 0.000, 0.000, 0.000, 0.000, 0.000).Levels of P-22, P13K, P-Fox01 and P-Fox03a in vastular tissue of group A were higher than group B, the differences were significant (P = 0.000, 0.000, 0.000, 0.000). Fistula thrombosis in patients with vascular tissue were significantly correlated with SOD-1, SOD-2, HO-1, Rac-2, NOX-4, P-22, P13K, P-Fox01 and P-Fox03a levels (P = 0.040, 0.010, 0.041, 0.022, 0.030, 0.021, 0.031, 0.020, 0.021). Conclusions The oxidative stress expresses protein associated enzymes by P13K/Fox0 signal transduction pathway, causes endothelial damage, leads to stenosis of arteriovenous fistula and anastomosis thrombosis. Clinical intervention by the stress response can move fistula patients intravenously and in vivo signaling pathway associated protein expression in the formation of prevention or treatment of arteriovenous fistula thrombosis.