Effects of Chlorich®EnergyBoost on Enhancing Physical Performance and Anti-Fatigue Properties in Mice.

Chlorich®EnergyBoost, a water extract obtained from Chlorella sorokiniana, has been proposed to enhance physical performance and provide anti-fatigue effects. This study assessed the impact of Chlorich®EnergyBoost supplementation on physical performance and its anti-fatigue properties. Twenty-four mice were allocated into four groups: (1) the control group receiving only water,;(2) the 1X group (49.2 mg/kg/day); (3) the 2X group (98.4 g/kg/day); and (4) the 5X group (246 g/kg/day). All groups were orally administered the supplements for four consecutive weeks. The evaluation included grip strength, swimming endurance, an exhaustion test, and serum biochemistry analysis. Additionally, the study examined the bioactive peptides through matrix-assisted laser desorption/ionization mass spectrometry (MALDI-TOF MS) and conducted bacterial reverse mutation and acute oral toxicity tests for safety assessment. The findings indicated that Chlorich®EnergyBoost supplementation led to a significant reduction in serum lactate levels by 14.08% to 22.54% and blood urea nitrogen levels by 12.23% to 16.76%, an increase in the lactate clearance rate by 0.28 to 0.35, an enhancement of muscle glycogen storage by 1.10 to 1.44-fold, and hepatic glycogen storage by 1.41 to 1.47-fold. These results demonstrated dose-dependent effects. MALDI-TOF analysis revealed the expression of dihydrolipoamide dehydrogenase and superoxide dismutase. Both the bacterial reverse mutation and acute oral toxicity tests showed no adverse effects.

Vitamin D retards intervertebral disc degeneration through inactivation of the NF-κB pathway in mice.

To determine the efficacy and specific mechanism of vitamin D on intervertebral disc degeneration. The model of intervertebral disc degeneration was established in 3-month-old mice. Furthermore, the levels of intervertebral disc degeneration in the vitamin D group and the control group were detected one month later by X-ray, Western boltting, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) et al. In addition, in vitro, we cultured mouse intervertebral disc nucleus pulposus cells to verify the effect of vitamin D on nucleus pulposus cells and study its mechanism. In vivo, compared with the control group, mice in the vitamin D group showed dose-dependent retardation of intervertebral disc degeneration in terms of reducing inflammatory responses, antioxidant stress, inhibiting apoptosis and delaying cell aging. In vitro, compared with the control group, collagen II was increased and collagen X was decreased in mice treated with vitamin D. In vivo and in vitro experiments, the expression of p65 and IκB kinase α was decreased and the expression of inhibitor of NF-κB was increased in the intervertebral disc tissue or nucleus pulposus cells of the vitamin D treatment group, indicating that vitamin D could suppress the NF-κB pathway. Vitamin D retarded intervertebral disc degeneration by inhibiting NF-κB pathway, which may relieve inflammatory reactions, resist oxidative stress, inhibit apoptosis and delay cell senescence.