醛类应激介导ω-3鱼油脂肪乳剂预处理减轻大鼠脑局灶性缺血再灌注损伤的机制研究

目的探究ω-3鱼油脂肪乳剂预处理对大鼠脑局灶性缺血再灌注损伤的保护作用，分析其可能机制。方法将40RSD大鼠随机分成正常组（C组）、模型组（M组）、ω-3鱼油脂肪乳剂5d组（FOFE-5组）、ω-3鱼油脂肪乳剂10d组（FOFE-10组）、02—3鱼油脂肪乳剂15d组（FOFE～15组），静脉尾注药物，并建立鼠脑局灶性缺血再灌注损伤模型，比较各组大鼠的神经行为评分、大脑梗死面积，脑组织中丙二醛（MDA）、乳酸脱氢酶（LHD）水平，核因子E2相关因子2（Nrf2）、血红素氧化酶Ho-1mRNA表达。结果c组大鼠的神经行为评分和大脑梗死面积均为0，FOFE-5、FOFE-10组以及FOFE-15组大鼠的神经行为评分和大脑梗死面积较M组显著降低；与M组比较，FOFE-5预处理使MDA、LHD水平显著降低；与c组比较，M组的大鼠脑组织中Nrt2和Ho-1mRNA相对表达量明显升高，FOFE-5预处理组的Nrf2和Ho—lmRNA相对表达量较M组明显升高，差异均具有显著性（P〈0．05）。结论ω-3鱼油脂肪乳剂预处理通过调节醛类应激介导的氧化应激以及Nrf2／HO-1信号通路对大鼠大脑局灶性缺血再灌注损伤起到了保护作用。

Objective To investigate the protective effect of ω-3 fish oil fat emulsion pretreatment on focal cerebral ischemia-repeffusion injury in rats, and to analyze its possible mechanism. Methods Forty SD rats were randomly divided into normal group （ group C ） , model group （ M group ） , omega-3 fish fat emulsion 5 days group （ FOFE-5 group ） ,ω-3 fish oil fat emulsion 10 days group （ FOFE - 10 groups ） , omega-3 fish oil fat emulsion 10 days group （ FOFE-15 group ） . Intravenous injection of the tail, and the establishment of rat brain focal ischemia-reperfusion injury, then the neurological score, cerebral infarction area, the levels of malondialdehyde （ MDA ） , lactate dehydrogenase （ LHD ） , Nff2 and HO-1 mRNA in brain tissue were compared. ResuRs The neurological score and brain infarct size of group C were all 0. Neurobehavioral score and cerebral infarction area in FOFE-5, FOFE-10 and FOFE-15 groups were significantly lower than those in group M compared with M group, FOFE- 5 pretreatment significantly decreased MDA and LHD levels compared with the C group, the expression of Nrf2 and HO-1 mlLNA in brain tissue of M group was significantly higher, and the expression of Nrf2 and HO-1 mRNA in FOFE-5 pretreatment group was significantly higher than that in group M. The difference were significant （ P〈0.05 ） . Conclusion Omega-3 fish oil fat emulsion pretreatment has a protective effect on focal cerebral ischemia- repeffusion injury in rats by the oxidative stress mediated by aldehyde stress and the Nrf2 / HO-1 signaling pathway.