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首页> 外文期刊>The Journal of Nutritional Biochemistry >Protective effect of docosahexaenoic acid against brain injury in ischemic rats
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Protective effect of docosahexaenoic acid against brain injury in ischemic rats

机译：二十二碳六烯酸对缺血大鼠脑损伤的保护作用

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摘要

Evidence suggests that inactivation of cell-damaging mechanisms and/or activation of cell-survival mechanisms may provide effective preventive or therapeutic interventions to reduce cerebral ischemia/reperfusion (I/R) injuries. Docosahexaenoic acid (DHA) is an essential polyunsaturated fatty acid in the central nervous system that has been shown to possess neuroprotective effects. We examined whether different preadministrative protocols of DHA have effects on brain injury after focal cerebral I/R and investigated the potential neuroactive mechanisms involved. Sprague-Dawley rats were intraperitoneally pretreated with DHA once 1 h or 3 days being subjected to focal cerebral I/R or daily for 6 weeks before being subjected to focal cerebral I/R. Reduction of brain infarction was found in all three DHA-pretreated groups. The beneficial effect of DHA on the treatment groups was accompanied by decreases in blood-brain barrier disruption, brain edema, malondialdehyde (MDA) production, inflammatory cell infiltration, interleukin-6 (IL-6) expression and caspase-3 activity. Elevation of antioxidative capacity, as evidenced by decreased MDA level and increased superoxide dismutase activity and glutathione level, was detected only in the chronic daily-administration group. The two single-administration groups showed increased phosphorylation of extracellular-signal-regulated kinase (ERK). Elevation of Bcl-2 expression was detected in the chronic daily-administration and 3-day-administration groups. In vitro study demonstrated that DHA attenuated IL-6 production from stimulated glial cells involving nuclear factor B inactivation. Therefore, the data suggest that the neuroprotective mechanisms of DHA pretreatment are, in part, mediated by attenuating damaging mechanisms through reduction of cytotoxic factor production and by strengthening survival mechanisms through ERK-mediated and/or Bcl-2-mediated prosurvival cascade.
机译：有证据表明，细胞破坏机制的失活和/或细胞存活机制的活化可提供有效的预防或治疗干预措施，以减少脑缺血/再灌注（I / R）损伤。二十二碳六烯酸（DHA）是中枢神经系统中必不可少的多不饱和脂肪酸，已显示具有神经保护作用。我们检查了不同的DHA预给药方案是否对局灶性脑I / R后的脑损伤有影响，并研究了潜在的神经活性机制。对Sprague-Dawley大鼠进行DHA腹膜内预处理1小时或3天，进行局灶性脑I / R，或每天进行6周，然后再进行局灶性脑I / R。在所有三个DHA预处理组中均发现脑梗塞减少。 DHA对治疗组的有益作用伴随着血脑屏障破坏，脑水肿，丙二醛（MDA）产生，炎性细胞浸润，白介素6（IL-6）表达和caspase-3活性降低。 MDA水平降低，超氧化物歧化酶活性和谷胱甘肽水平升高证明了抗氧化能力的提高，仅在慢性每日给药组中才发现。两个单次给药组显示细胞外信号调节激酶（ERK）的磷酸化增加。在慢性每日给药组和3天给药组中检测到Bcl-2表达升高。体外研究表明，DHA减弱了涉及核因子B失活的受刺激神经胶质细胞的IL-6产生。因此，数据表明，DHA预处理的神经保护机制部分是通过减少细胞毒性因子的产生来减弱伤害机制，以及通过ERK介导的和/或Bcl-2介导的生存级联来增强生存机制来介导的。

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