Oxidative stress of neurons caused by a series of complex neuropathological processes will induce certain neurodegenerative disorders including epilepsy. Curcumin (Cur) is an effective natural antioxidant compound; however, the poor bioavailability obstructs its neural protective applications. In this study, Cur is encapsulated in solid lipid nanoparticles (SLNs) for better neuroprotective efficacy. In vitro study certified that Cur-SLNs functioned obviously better against neuronal apoptosis than Cur, by significantly decreasing the level of free radical and reversing mitochondrial function through the activation of the Bcl-2 family. In vivo experiments showed that SLNs transported Cur through the blood–brain barrier (BBB). The behavioral performance of epileptic mice was improved by Cur-SLNs, with more NeuN but less TUNEL positive cells observed in hippocampus. The in vivo mechanism was also explored. Cur-SLNs reduced neuronal apoptosis through Bcl2 family and P38 MAPK pathways. Overall, Cur-SLNs have better protective effects toward oxidative stress in neurons than free Cur both in vitro and in vivo, which suggests they may be a promising agent against neurodegenerative disorders including epilepsy.

中文翻译：

---

固体脂质纳米颗粒通过激活 Bcl-2 家族和 P38 MAPK 通路增强姜黄素对癫痫的神经保护作用。

由一系列复杂的神经病理过程引起的神经元氧化应激会诱发某些神经退行性疾病，包括癫痫。姜黄素 (Cur) 是一种有效的天然抗氧化化合物；然而，较差的生物利用度阻碍了其神经保护应用。在这项研究中，Cur 被包裹在固体脂质纳米颗粒 (SLN) 中，以获得更好的神经保护功效。体外研究证明，Cur-SLNs 通过显着降低自由基水平和通过激活 Bcl-2 家族逆转线粒体功能，对神经元凋亡的作用明显优于 Cur。体内实验表明，SLNs 通过血脑屏障 (BBB) 转运 Cur。Cur-SLNs 改善了癫痫小鼠的行为表现，在海马中观察到更多的 NeuN 但较少的 TUNEL 阳性细胞。还探讨了体内机制。Cur-SLNs 通过 Bcl2 家族和 P38 MAPK 通路减少神经元凋亡。总体而言，在体外和体内，Cur-SLNs 对神经元氧化应激的保护作用比游离 Cur 更好，这表明它们可能是对抗包括癫痫在内的神经退行性疾病的有前途的药物。