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DOI: 10.1055/s-0037-1608047
Effects of Cimicifuga Extract Ze 450 on mitochondrial resilience
Publication History
Publication Date:
24 October 2017 (online)
Cimicifuga racemosa extract is currently used in the therapy of menopausal symptoms. The mechanisms of Cimicifuga extract underlying its multiple therapeutic effects are not well defined. Recent studies showed that Cimicifuga extract Ze 450 activates AMP-activated protein kinase suggesting beneficial metabolic effects, e.g. for the treatment of type II diabetes [1]. In the pathogenesis of metabolic, immunological and age-related diseases, mitochondrial dysfunction is an emerging focus of research, since these organelles are key regulators of energy metabolism and cellular homeostasis. Increasing evidence suggests that mitochondrial resilience can provide protection against age-related pathologies [2].
In this study, we investigated the effects of Ze 450 (1 – 200 µg/ml) on mitochondrial integrity and function, and cell viability in models of oxidative stress in neuronal cell lines and in liver cells. The effects of Ze 450 in control conditions and after oxidative stress were analyzed using FACS for detecting lipid peroxidation (BODIPY), mitochondrial ROS formation (MitoSOX) and cell death (AnnexinV/PI staining). Furthermore, we determined ATP levels and mitochondrial respiration (oxygen consumption rates; Seahorse).
In the models of oxidative stress, Ze 450 (50 – 200 µg/ml) preserved mitochondrial morphology, ATP levels, and prevented mitochondrial ROS formation and cell death in neuronal cells. Further, cell death was remarkably inhibited by Ze 450 in a dose-dependent manner in liver cells, whereas under standard culture conditions Ze 450 itself did not affect liver or neuronal cell viability.
In conclusion, our data show that Cimicifuga extract Ze 450 did not affect cell viability under control conditions and supported mitochondrial resilience and preserved cell viability in neuronal and liver cells exposed to oxidative stress. Therefore, Ze 450 offers promising therapeutic potential in ageing processes and related diseases involving mitochondrial damage and increased ROS formation.
[1] Moser C. et al, Phytomedicine. 2014; 21: 1382 – 1389
[2] Held N.M. et al, Bioessays. 2015; 37: 867 – 876