Abstract
EstroG-100®, a functional ingredient blend that has been used for menopausal health in women. However, detailed studies on its effects and their underlying mechanisms have been lacking. Herein, we evaluated the antifatigue effects of EstroG-100 using C2C12 cells exposed to oxidative stress and mice subjected to a forced swimming test. EstroG-100 significantly increased the viability and adenosine triphosphate (ATP) content of C2C12 cells under oxidative stress, while notably inhibiting the generation of reactive oxygen species. EstroG-100 tended to prolong the forced swimming time in mice. It also significantly inhibited the serum lactate dehydrogenase activity, increased intramuscular glycogen content, and upregulated the expression of peroxisme proliferator-activated receptor (PPAR)-δ and uncoupling protein (UCP)3 genes involved in β-oxidation of fatty acids. Furthermore, EstroG-100 significantly increased the activities of antioxidant enzymes, including catalase, superoxide dismutase, glutathione S-transferase, and glutathione levels, and decreased the malondialdehyde levels in the liver. These results indicate that EstroG-100 may contribute to recovery from physical fatigue by enhancing the antioxidant activity to alleviate oxidative stress and improving muscle function via modulation of glycogen and fatty acid metabolism.
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