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Background  Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, but there is still no effective way to stop or slow its progression. Our previous studies demonstrated that extract of  Cynomorium songaricum  (ECS), a Chinese herbal medicine, had neuroprotective effects in AD models in vivo. However, the pharmacological mechanism of ECS in AD is still unclear.    Methods  To study the mechanisms of action of the effects of ECS on AD, we used Aβ 25–35-  and H 2 O 2 -exposed HT22 cells to mimic specific stages of AD in vitro. The mitochondrial membrane potential (MMP), intracellular ATP, intracellular reactive oxygen species (ROS), and expression levels of mitochondrial dynamics-related proteins in each group were examined. Furthermore, we explored the mechanisms by which ECS reduces the phosphorylation of Drp1 at Ser637 and the changes in the concentrations of intracellular calcium ions in the two models after FK506 intervention.    Results  The results showed that ECS significantly enhanced the MMP ( P  < 0.05), increased intracellular ATP levels (P < 0.05) and decreased intracellular ROS levels in the Aβ- and H 2 O 2 -induced cell models ( P  < 0.05). Additionally, ECS regulated the expression levels of mitochondrial dynamics-related proteins by reducing the phosphorylation of Drp1 at Ser637 ( P  < 0.05) and decreasing the expression of Fis1 in the H 2 O 2 -induced models ( P  < 0.05). Further study indicated that ECS reduced the overload of intracellular calcium ( P  < 0.05).    Conclusion  Our study results suggest that ECS protects the mitochondrial ultrastructure, ameliorates mitochondrial dysfunction, and maintains mitochondrial dynamics in AD models.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12906-021-03375-2.

bmc complementary medicine and therapies

Extract of Cynomorium songaricum ameliorates mitochondrial ultrastructure impairments and dysfunction in two different in vitro models of Alzheimer’s disease