In vivo longitudinal proton magnetic resonance spectroscopy on neonatal hypoxic-ischemic rat brain injury: Neuroprotective effects of acetyl-L-carnitine.
In vivo longitudinal proton magnetic resonance spectroscopy on neonatal hypoxic-ischemic rat brain injury: Neuroprotective effects of acetyl-L-carnitine.
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DOI：
10.1002/mrm.25537
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发表时间：
2015-12
影响因子：
3.3
通讯作者：
Gullapalli, Rao P.
中科院分区：
文献类型：
--
作者：
Xu, Su;Waddell, Jaylyn;Zhu, Wenjun;Shi, Da;Marshall, Andrew D.;McKenna, Mary C.;Gullapalli, Rao P.
关键词：
本研究采用活体质子短程点分辨光谱分析方法，评价新生大鼠缺氧缺血(HI)后的纵向代谢变化，并检测乙酰化L肉碱(ALCAR)的神经保护作用。在7日龄SD大鼠上建立了莱斯-万努奇模型。分别于缺氧缺血后24 h、72 h、7 d、28 d 4个时间点的对侧和同侧大脑皮质、海马区取材。分别于伤后即刻、伤后4小时、24小时、48小时皮下注射ALCAR(100 mg/kg)。与对照组相比，损伤后24小时，HI大鼠同侧海马区谷胱甘肽(p<；0.005)、肌醇(p<；0.002)、牛磺酸(p<；0.001)和总肌酸(p<；0.005)显著降低。ALCAR治疗的HI大鼠与单纯HI大鼠相比，在24小时内乳酸水平较低，总肌酸水平保持不变，病变面积较小。在损伤后24小时，HI幼鼠的同侧海马区出现严重的氧化、渗透应激、磷酸化受损和无氧糖酵解倾向。如果在HI后早期给予ALCAR作为能量底物，并促进氧化大脑能量的产生和最大限度地减少无氧糖酵解，则似乎具有神经保护作用。
This study evaluated the longitudinal metabolic alterations after neonatal hypoxia-ischemia (HI) in rats and tested the neuroprotective effect of acetyl-L-carnitine (ALCAR) using in vivo proton short-TE Point-RESolved Spectroscopy method. Rice-Vannucci model was used on 7-day-old Sprague-Dawley rats. Data were acquired from contralateral and ipsilateral cortex and hippocampus, respectively at 4 time points (24-h, 72-h, 7-d, 28-d) post-HI. The effect of subcutaneous administration of ALCAR (100 mg/kg) immediately after HI, at 4-h, 24-h, and 48-h post-HI was determined. Significant reductions in glutathione (p < 0.005), myo-inositol (p < 0.002), taurine (p < 0.001), and total creatine (p < 0.005) were observed at 24-h post injury compared to the control group in the ipsilateral hippocampus of the HI rat pups. ALCAR-treated-HI rats had lower levels of lactate and maintained total creatine at 24-h and had smaller lesion size compared to the HI only rats. Severe oxidative, osmotic stress, impaired phosphorylation, and a preference for anaerobic glycolysis were found in the ipsilateral hippocampus in the HI pups at 24-h post injury. ALCAR appeared to have a neuroprotective effect if administered early after HI by serving as an energy substrate and promote oxidative cerebral energy producing and minimize anaerobic glycolysis.
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