Maca has attracted considerable attention owing to its neuroprotective effects in vitro and vivo . Macamides, a series of nonpolar and long-chain fatty acid N -benzylamides, are considered unique constituents in maca. This study investigated the protective effects of ethanol extracts of maca (EEM) and macamides on corticosterone-induced (CORT) neurotoxicity in rat pheochromocytoma (PC12) cells. CORT reduced cell viability and increased LDH release, intracellular ROS levels, and MMP decline rate, and induced mitochondrial apoptosis. However, pretreatment with EEM and macamides ameliorated CORT-induced neurotoxicity. EEM increased the cell viability and reduced the LDH release. M 18:1, M 18:2, and M 18:3 increased cell viability and reduced LDH release and intracellular ROS generation. M 18:2 and M 18:3 inhibited MMP reduction and reduced the Bax/Bcl-2 ratios. M 18:1 reduced the intracellular ROS without affecting other factors. Moreover, M 18:3 prevented CORT-induced mitochondrial apoptosis, restrained the expression levels of pro-apoptotic proteins, namely, Bax, cytochrome C, cleaved-caspase-3, and cleaved-PARP, and increased the expression levels of Bcl-2. In addition, M 18:3 increased Akt phosphorylation and the ability of M 18:3 to protect against CORT-induced cytotoxicity was remarkably reduced by LY294002, a PI3K phosphorylation inhibitor. M 18:3 also elevated the phosphorylation of CREB and activated the BDNF protein levels in CORT-induced PC12 cells. In conclusion, macamides, especially M 18:3, exert protective effects on CORT-induced PC12 cells. The cellular mechanism of M 18:3 against CORT-induced cytotoxicity may involve inhibition of mitochondrial apoptosis, and activation of Akt and CREB phosphorylation. Overall, macamides may potentially treat neuronal damage induced by CORT.
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机译：由于其在体外和体内的神经保护作用，玛卡已经引起了相当大的关注。玛酰胺是一系列非极性和长链脂肪酸N-苄基酰胺，被认为是玛咖中的独特成分。这项研究调查了玛卡乙醇提取物（EEM）和甲酰胺对大鼠嗜铬细胞瘤（PC12）细胞中皮质酮诱导（CORT）神经毒性的保护作用。 CORT降低细胞活力并增加LDH释放，细胞内ROS水平和MMP下降率，并诱导线粒体凋亡。但是，EEM和甲酰胺的预处理可以改善CORT诱导的神经毒性。 EEM增加了细胞活力并减少了LDH的释放。 M 18：1，M 18：2和M 18：3增加细胞活力，减少LDH释放和细胞内ROS生成。 M 18：2和M 18：3抑制MMP降低并降低Bax / Bcl-2比。 M 18：1在不影响其他因素的情况下降低了细胞内ROS。此外，M 18：3阻止了CORT诱导的线粒体凋亡，抑制了促凋亡蛋白Bax，细胞色素C，裂解的caspase-3和裂解的PARP的表达水平，并增加了Bcl-2的表达水平。 。此外，PI 3K磷酸化抑制剂LY294002显着降低了M 18：3增加的Akt磷酸化，并且M 18：3抵抗CORT诱导的细胞毒性的能力显着降低。 M 18：3还提高了CORT诱导的PC12细胞中CREB的磷酸化并激活了BDNF蛋白水平。总之，甲酰胺，特别是M 18：3，对CORT诱导的PC12细胞具有保护作用。 M 18：3对抗CORT诱导的细胞毒性的细胞机制可能包括抑制线粒体凋亡，激活Akt和CREB磷酸化。总体而言，甲酰胺可能潜在地治疗CORT诱导的神经元损伤。
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