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https://www.selleckchem.com/products/sodium-ascorbate.html Interestingly, the animals treated with mixed doses of Ag-NPs and YO-NPs displayed improvements in behavioral tests, oxidative parameters, and neurotransmitters compared to males treated with Ag-NPs alone. In conclusion, the abnormal behavior related to learning and memory in male mice induced by Ag-NPs was significantly alleviated by YO-NPs. Specifically, the coinjection of YO-NPs with Ag-NPs moderates the disruption in neurotransmitters, oxidative indices of mice brains, which reflects on their cognitive behaviors.Current evidences indicate that both inflammation and oxidative stress contribute to the pathogenesis of sepsis-associated skeletal muscle atrophy. However, the interaction between inflammation and oxidative stress has not been completely understood in sepsis-associated skeletal muscle atrophy. Here in the present study, a murine model of sepsis has been established by cecal ligation and puncture (CLP) with wild-type and interleukin- (IL-) 6 knockout (KO) mice. Our results suggested that IL-6 KO largely attenuated skeletal muscle atrophy as reflected by reduced protein degradation, increased cross-sectional area (CSA) of myofibers, and improved muscle contractile function (all P less then 0.05). In addition, we observed that IL-6 KO promoted the expression of peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and inhibited CLP-induced mitochondrial reactive oxygen species (ROS) production in skeletal muscles (all P less then 0.05). However, the knockdown of PGC-1α abolished the protective effects of IL-6 KO in CLP-induced skeletal muscle atrophy and reversed the changes in mitochondrial ROS production (all P less then 0.05). Ex vivo experiments found that exogenous IL-6 inhibited PGC-1α expression, promoted mitochondrial ROS production, and induced proteolysis in C2C12 cells (all P less then 0.05). Together, these results suggested that IL-6 deficiency attenuated skeletal mu

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