摘要
AIM： TO investigate the effect of exogenous erythro- poietin （EPO） administration on acute lung injury （ALI） in an experimental model of sodium taurodeoxycholate- induced acute necrotizing pancreatitis （ANP）. METHODS： Forty-seven male Wistar albino rats were randomly divided into 7 groups： sham group （n = 5）, 3 ANP groups （n = 7 each） and 3 EPO groups （n = 7 each）. ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum arnilase, IL-2, IL-6 and lung tissue malondialdehyde （MDA） were measured. Pleural effusion volume and lung/body weight （LW/BW） ratios were calculated. Tissue levels of TNF-a, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored.RESULTS： The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-（~ （TNF-（~） and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters a^er exogenous EPO administration, particularly at 48 h and 72 h. CONCLUSION： EPO administration leads to a significant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte （PMNL） accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI.
瞄准：为了调查外长的 erythro-poietin (EPO ) 的效果，在钠 taurodeoxycholate- 的一个试验性的模型的尖锐的肺损害(ALI ) 上的管理导致了尖锐引起坏死胰腺炎(ANP ) 。方法：47 只男 Wistar 白鼠随机被划分成 7 个组：假冒的组(n = 5 ) ， 3 个 ANP 组(n = 7 各个) 并且 3 个 EPO 组(n = 7 各个) 。ANP 被导致由后退进胆总管的 5% 钠 taurodeoxycholate 的注入。在 EPO 组的老鼠收到了 1000 U/kg 肌内的 EPO 立即在 ANP 的正式就职以后。在 ANP 组的老鼠相反被给 1 mL 生理盐水。所有动物被牺牲在手术后 24 h， 48 h 和 72 h。浆液 amilase， IL-2， IL-6 和肺织物 malondialdehyde (MDA ) 被测量。胸膜渗漏体积和肺 / 身体重量(LW/BW ) 比率是计算的。TNF-alpha， IL-2 和 IL-6 的织物层次组织化学地是屏蔽免疫。另外， ox-LDL 累积与免疫者荧光灯的染色被估计。在肺的组织病理学说的改变也被获得。结果：吝啬的胸膜渗漏体积，计算 LW/BW 比率，浆液 IL-6 和肺织物 MDA 层次比在 ANP 组在 EPO 组是显著地更低的。不，统计上，有效差量在这些组之中在浆液或 IL-2 的织物价值被观察。当时， ox-LDL 的肿瘤坏死 factor-alpha (TNF-alpha ) 和 IL-6 和累积的水平在 ANP 组的肺纸巾是明显的与 EPO 组相比，特别地在 72 h。组织病理学说的评估在外长的 EPO 管理以后在肺损害参数证实了改进，特别地在 48 h 和 72 h。结论：EPO 管理由禁止 polymorphonuclear (PMNL ) 在 ALI 参数导致重要减少累积，减少专业版的层次在每氧化的循环，保存微脉管的内皮房间正直和减少的氧化联系压力的类脂化合物的煽动性的 cytokines 并且因此，能在导致 ANP 的 ALI 被认为是一个 cytoprotective 代理人。
