Aconitine is a crucial toxic component in Chinese herbal medicines such as Aconitum, Aconitum coreanum, and Aconitum soongaricum. The poisoning symptoms of the central nervous system and cardiovascular system caused by it are relatively common in China, and there are many studies on cardiovascular system diseases caused by aconitine. However, the specific mechanism of neurotoxicity induced by aconitine is still unclear. This study explored the effect and mechanism of mitochondrial calcium uniporter on mitochondrial energy metabolism disorder in aconitine poisoning hippocampal neurons. The results showed that after treatment with 400μmol/L aconitine, mitochondrial energy metabolism was abnormal in rat hippocampal neuron cells, the expression of MCU in mitochondria was up-regulated, calcium overload in mitochondria, ATP production decreased, and mitochondrial membrane potential Changes, increased expression of the apoptosis gene Cleaved-Caspase-3. After treatment with the MCU agonist spermine, mitochondrial energy metabolism was significantly abnormal, and cell apoptosis was increased considerably. However, pretreatment with calcium ion channel inhibitor Ruthenium Red (RR) effectively promoted the generation of ATP, thereby improving mitochondrial energy metabolism disorders and reducing cell apoptosis. These results suggest that aconitine induces mitochondrial energy metabolism dysfunction in hippocampal neurons, which may be related to the increased expression of MCU.

乌头碱是乌头、乌头、乌头等中药材中的重要有毒成分。其引起的中枢神经系统和心血管系统中毒症状在我国较为常见，关于乌头碱引起的心血管系统疾病的研究也较多。但乌头碱引起神经毒性的具体机制尚不清楚。本研究探讨线粒体钙单向转运蛋白对乌头碱中毒海马神经元线粒体能量代谢紊乱的影响及机制。结果显示，400μmol/L乌头碱处理后，大鼠海马神经元细胞线粒体能量代谢异常，线粒体中MCU表达上调，线粒体钙超载，ATP产生减少，线粒体膜电位变化、增加凋亡基因 Cleaved-Caspase-3 的表达。MCU激动剂精胺处理后，线粒体能量代谢明显异常，细胞凋亡明显增加。然而，钙离子通道抑制剂钌红（RR）预处理有效促进了ATP的生成，从而改善线粒体能量代谢紊乱，减少细胞凋亡。这些结果表明乌头碱诱导海马神经元线粒体能量代谢功能障碍，这可能与MCU表达增加有关。