Oxidative stress plays a key role in the degeneration of dopaminergic neurons in Parkinson’s disease (PD), which may be aggravated by concomitant PD-associated gut dysbiosis. Probiotics and prebiotics are therapeutically relevant to these conditions due to their antioxidant, anti-inflammatory, and gut microbiome modulation properties. However, the mechanisms by which probiotic/prebiotic supplementation affects antioxidant capacity and the gut microbiome in PD remains poorly characterized. In this study, we assessed the effects of a Lactobacillus salivarius AP-32 probiotic, a prebiotic (dried AP-32 culture medium supernatant), and a probiotic/prebiotic cocktail in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced PD. The neuroprotective effects and levels of oxidative stress were evaluated after eight weeks of daily supplementation. Fecal microbiota composition was analyzed by fecal 16S rRNA gene sequencing. The supplements were associated with direct increases in host antioxidant enzyme activities and short-chain fatty acid production, protected dopaminergic neurons, and improved motor functions. The supplements also altered the fecal microbiota composition, and some specifically enriched commensal taxa correlated positively with superoxide dismutase, glutathione peroxidase, and catalase activity, indicating supplementation also promotes antioxidant activity via an indirect pathway. Therefore, L. salivarius AP-32 supplementation enhanced the activity of host antioxidant enzymes via direct and indirect modes of action in rats with 6-OHDA-induced PD.
In this study, we investigated the anticancer effect of protoapigenone on human prostate cancer cells. Protoapigenone inhibited cell growth through arresting cancer cells at S and G 2 /M phases as well as inducing apoptosis. Blockade of cell cycle by protoapigenone was associated with an increase in the levels of inactivated phospho (p)-Cdc25C (Ser 216 ) and a decrease in the levels of activated p-cyclin B1 (Ser 147 ), cyclin B1, and cyclindependent kinase (Cdk) 2. Protoapigenone triggered apoptosis by increasing the levels of cleaved poly(ADP-ribose) polymerase and caspase-3. In addition, activation of p38 mitogenactivated protein kinase (MAPK) and c-Jun NH 2 -terminal kinase (JNK)1/2 was a critical mediator in protoapigenone-induced cell death. Inhibition of the expression of p38 MAPK and JNK1/2 by pharmacological inhibitors or specific small interfering RNA reversed the protoapigenone-induced apoptosis through decreasing the level of cleaved caspase-3. In contrast, p38 MAPK, but not JNK1/2, was involved in the protoapigenonemediated S and G 2 /M arrest by modulating the levels of Cdk2 and p-Cdc25C (Ser 216 ). Moreover, in vivo xenograft study showed that protoapigenone had a significant inhibition of prostate tumor growth without major side effects on the mice we tested. This inhibition was associated with induction of apoptosis and activation of p38 MAPK and JNK1/2 in protoapigenone-treated tumor tissues. In conclusion, our results demonstrated protoapigenone suppressed prostate cancer cell growth through the activation of p38 MAPK and JNK1/2, with the potential to be developed as a chemotherapeutic agent for prostate cancer.
Bifidobacterium longum subsp. longum Olympic No. 1 (OLP-01) has been shown in previous animal experiments to improve exercise endurance performance, but this effect has not been confirmed in humans, or more particularly, in athletes. Toward this end, the current study combined OLP-01 supplementation with regular exercise training in well-trained middle- and long-distance runners at the National Taiwan Sport University. The study was designed as a double-blind placebo-controlled experiment. Twenty-one subjects (14 males and seven females aged 20–30 years) were evenly distributed according to total distance (meters) traveled in 12 min to one of the following two groups: a placebo group (seven males and three females) and an OLP-01 (1.5 × 1010 colony forming units (CFU)/day) group (seven males and four females). All the participants received placebo or OLP-01 supplements for five consecutive weeks consisting of three weeks of regular training and two weeks of de-training. Before and after the experiment, the participants were tested for 12-min running/walking distance, and body composition, blood/serum, and fecal samples were analyzed. The results showed that OLP-01 significantly increased the change in the 12-min Cooper’s test running distance and the abundance of gut microbiota. Although no significant change in body composition was found, OLP-01 caused no adverse reactions or harm to the participants’ bodies. In summary, OLP-01 can be used as a sports nutrition supplement, especially for athletes, to improve exercise performance.
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