Mito-Tempo is a mitochondria-targeted antioxidant with effective superoxide scavenging properties, which converts toxic superoxide molecules into hydrogen peroxide or oxygen and subsequently detoxified to oxygen and water by catalase or glutathione peroxidase[1].
In vitro, Mito-Tempo has a greater protective effect by enhancing superoxide dismutase (SOD) activity and PI3K/AKT/mTOR phosphorylation. Glutamate-exposed cells significantly increased cellular oxidative stress by enhancing ROS production. Glutamate treatment also increased LDH release follows the loss of mitochondrial membrane potential, caused cell viability loss. Treatment with Mito-Tempo not only attenuated the generation of ROS and improved mitochondrial membrane potential but also reduced the neurotoxicity of glutamate in a concentration-dependent manner, which leads to increased cell viability and decreased LDH release[2]
In vivo，Mito-TEMPO pretreatment inhibited inflammation, attenuated LPS-induced liver injury, and enhanced the antioxidative capability in septic mice, as evidenced by the decreased MDA content and the increased SOD activity. In addition, Mito-TEMPO restored mitochondrial size and improved mitochondrial function. Finally, we found that the levels of pyroptosis-related proteins in the liver of LPS-treated mice were lower after pretreatment with Mito-TEMPO [3]
References:
[1]. Liang HL, Sedlic F, et al. SOD1 and MitoTEMPO partially prevent mitochondrial permeability transition pore opening, necrosis, and mitochondrial apoptosis after ATP depletion recovery. Free Radic Biol Med. 2010 Nov 30;49(10):1550-60.
[2]. Mukem S, Thongbuakaew T, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310.
[3]. Mukem S, Thongbuakaew T, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310.
Mito-Tempo 是一种靶向线粒体的抗氧化剂，具有有效的超氧化物清除特性，可将有毒的超氧化物分子转化为过氧化氢或氧气，随后通过过氧化氢酶或谷胱甘肽过氧化物酶解毒为氧气和水[1] .
在体外，Mito-Tempo 通过增强超氧化物歧化酶 (SOD) 活性和 PI3K/AKT/mTOR 磷酸化而具有更强的保护作用。暴露于谷氨酸的细胞通过增强 ROS 的产生显着增加细胞氧化应激。谷氨酸处理还增加了线粒体膜电位丧失后 LDH 的释放，导致细胞活力丧失。 Mito-Tempo 处理不仅减少了 ROS 的产生并改善了线粒体膜电位，而且以浓度依赖性方式降低了谷氨酸的神经毒性，从而导致细胞活力增加和 LDH 释放减少[2]
在体内，Mito-TEMPO 预处理可抑制炎症，减轻 LPS 诱导的肝损伤，并增强脓毒症小鼠的抗氧化能力，这可以通过降低 MDA 含量和增加 SOD 活性来证明。此外，Mito-TEMPO 恢复了线粒体大小并改善了线粒体功能。最后，我们发现在用 Mito-TEMPO [3]
预处理后，LPS 处理的小鼠肝脏中焦亡相关蛋白的水平较低