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.