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[重复低氧预处理对大鼠肾缺血再灌注诱导的肝功能障碍的影响]

[Effect of repeated hypoxic preconditioning on renal ischemia-reperfusion-induced hepatic dysfunction in rats].

作者信息

Yan Na, Feng Ze-Guo, Yan Guang-Tao, Yue Jian-Hong, Zhao Yan-Jun, Geng Na

机构信息

Anesthesia and Operation Center, Chinese PLA General Hospital, Beijing 100853, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2015 Jan;35(1):149-53.

PMID:25613631
Abstract

OBJECTIVE

To explore the effect of repeated hypoxic preconditioning (RHP) on renal ischemia-reperfusion-induced hepatic dysfunction in rats and the underlying mechanism.

METHODS

A total of 120 normal SD rats were randomly divided into 4 groups (n=40), namely RHP surgical group, RHP sham-operated (RHPS) group, nonhypoxic surgical group (IRI group), and nonhypoxic sham-operated group (S group). The rats in the hypoxic groups were exposed to hypoxia in a hypoxic chamber for 5 days prior to establishment of renal ischemia-reperfusion model by resection of the right kidney and clamping the left renal hilum. Serum alanine aminotransferase (ALT), IL-17 A, TNF-a, liver superoxide dismutase (SOD) and nitric oxide (NO) were detected at 2, 8 and 24h after reperfusion, and Western blotting was used to determine the expression of p-PI3K and p-AKT;HE staining was used to observe the structural changes in the liver.

RESULTS

Compared with IRI group, RHP group showed significantly milder hepatic damage, lower ALT levels and higher NO levels at 2, 8, and 24 after reperfusion (P<0.05); TNF-a levels were lowered at 24 h (P<0.05) and SOD increased at 8 h after the reperfusion (P<0.05). Compared with S group, IRI group and RHP group showed significantly higher IL-17A levels (P<0.05) but without significant difference between the latter two groups (P>0.05). The expressions of p-PI3K and P-Al<t in RHP group were significantly higher than those in IRI group (P<0.05), especially at 8 h after reperfusion (P<0.05).

CONCLUSION

Repeated hypoxic preconditioning can attenuate hepatic injury induced by renal ischemia-reperfusion injury in rats.

摘要

目的

探讨重复低氧预处理(RHP)对大鼠肾缺血再灌注诱导的肝功能障碍的影响及其潜在机制。

方法

将120只正常SD大鼠随机分为4组(n = 40),即RHP手术组、RHP假手术(RHPS)组、非低氧手术组(IRI组)和非低氧假手术组(S组)。低氧组大鼠在通过切除右肾并夹闭左肾蒂建立肾缺血再灌注模型前,于低氧舱内暴露于低氧环境5天。再灌注后2、8和24小时检测血清丙氨酸氨基转移酶(ALT)、IL-17A、TNF-α、肝脏超氧化物歧化酶(SOD)和一氧化氮(NO),并采用蛋白质免疫印迹法测定p-PI3K和p-AKT的表达;采用苏木精-伊红(HE)染色观察肝脏结构变化。

结果

与IRI组相比,RHP组在再灌注后2、8和24小时肝损伤明显较轻,ALT水平较低,NO水平较高(P<0.05);TNF-α水平在24小时降低(P<0.05),SOD在再灌注后8小时升高(P<0.05)。与S组相比,IRI组和RHP组IL-17A水平明显较高(P<0.05),但后两组之间无显著差异(P>0.05)。RHP组p-PI3K和p-AKT的表达明显高于IRI组(P<0.05),尤其是在再灌注后8小时(P<0.05)。

结论

重复低氧预处理可减轻大鼠肾缺血再灌注损伤诱导的肝损伤。

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