ω-3PUFA对颅脑损伤伴休克大鼠继发性肝损伤的保护作用

Protective effects of ω-3PUFA on the second liver injury in rats with traumatic brain injury and hemorrhagic shock

目的研究ω-3多不饱和脂肪酸（ω-3PUFA）对颅脑损伤伴失血性休克（TBIS）大鼠继发肝损伤的保护作用，并探讨相关机制。方法Wistar大鼠36只，随机（随机数字法）分成假手术组（c组）、TBIS模型组和ω-3PUFA治疗组，每组12只。检测血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）及肿瘤坏死因子（TNF）-a和肝组织超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽（GSH）的水平；观察肝组织病理学改变。结果与C组比较，TBIS组与ω-3PUFA治疗组血清ALT、AST及TNF-a水平与肝组织匀浆MDA水平明显升高（P〈0．01）；肝组织匀浆SOD及GSH水平均明显降低（P〈0．01）。与TBIS组比较，（ω-3PUFA治疗组血清ATJT、AST及TNF-a水平，肝组织匀浆MDA水平均明显降低（P〈0．01或P〈0．05），肝组织SOD及GSH水平均明显升高（P〈0．01或P〈0．05）。病理学检查可见TBIS组肝组织形态受损明显，ω-3PUFA治疗组肝组织受损较小。结论ω-3PUFA预处理可减轻TBIS大鼠继发性肝损伤，可能与其抑制氧自由基产生及促炎细胞因子的释放有关。

Objective To investigate the effects of preconditioning with ω-3 polyunsaturated fatty acid （ω-3 PUFA ） on the second liver injury in rats with traumatic b rain injury and hemorrhagic shock （TBIS） and explore the underlying mechanism. Methods Total of 36 male Wistar rats were assigned randomly （ random number） into 3 groups （ n = 12 in each） ： sham operation group （C） , TBIS model group and PUFA pretreatment group. The arterial blood samples were taken for determination of serum levels of ALT, AST and TNF-a. The liver were removed for determination of levels of superoxidc dismutase （SOD） , malondialdehyde （MDA） and glutathione （GSH） , and microscopic examination. Results Compared with group C, the serum levels of ALT, AST and TNF-ct and the liver levels of MDA were significantly higher （ P 〈 0. 01 ）, but the liver levels of SOD and GSH in group TBIS and group PUFA were significantly lower （ P 〈 0. 01 ）. The serum levels of ALT, AST and TNF-aand the liver levels of MDA were significantly lower （ P 〈 0. 01 or P 〈 0.05 ）, but the levels of SOD and GSH in liver tissues were significantly higher （ P 〈 0. 01 or P 〈 0.05 ） in group PUFA than those in group TBIS. Histological examination revealed the injury of liver in TBIS group, and the rats in PUFA treated group showed alleviated severity of liver injury. Conclusions The supplementation of ω-3 PUFA can ameliorate acute liver injury in rats with TBIS, which may contribute to inhibition of oxygen free radicals and inflammatory cytokines expression.