The effect and mechanism of 19S proteasome PSMD11/Rpn6 subunit in D-Galactose induced mimetic aging models

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-Mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

“…OS has long been implicated as a potential proximal physiological cost of reproduction during the lifespan of individuals ( Ikram et al, 2021 ). It has been confirmed that OS is determined by a negative regulator of ROS and has long been thought to be one of the most significant elements to be considered in accelerating chronic disease progression, such as Alzheimer’s and Parkinson’s disease, diabetes, aging, cancer, muscular dystrophy and heart disease ( Lu et al, 2010 ; Wu et al, 2020a ). To evaluate the antioxidant capacity of UB, we measured the scavenging rates of four kinds of free radicals, DPPH, ABTS + , O 2 − and OH − , which are commonly used to measure the total antioxidant capacity of chemical drugs and natural products.…”

“…AGEs are the major resources of ROS and can further promote free radical generation, thereby impacting the function of biological systems ( Chen et al, 2019 ). Evidence for the presence of a large body of aging models has verified that continuous chronic administration of a low dose of D-gal can produce aging-associated AD-like performance, including a disruption of deficits in learning and spatial memory, synaptic damage, neuronal loss, reduced activities of antioxidant enzymes and increased production of ROS ( Lu et al, 2010 ; Wu et al, 2020a ). Similarly, recent studies have shown that neuronal cell death is caused by a strengthened OS and could exacerbate motor and cognitive behavioral deficits ( Bracko et al, 2020 ).…”

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

“…Radical scavenging ability of UB in vitro OS has long been implicated as a potential proximal physiological cost of reproduction during the lifespan of individuals [5]. It has been con rmed that OS is determined by a negative regulator of ROS and has long been thought to be one of the most signi cant elements to be considered in accelerating chronic disease progression, such as Alzheimer's and Parkinson's disease, diabetes, aging, cancer, muscular dystrophy and heart disease [8,9]. To evaluate the antioxidant capacity of UB, we measured the scavenging rates of four kinds of free radicals, DPPH, ABTS + , O 2 and OH -, which are commonly used to measure the total antioxidant capacity of chemical drugs and natural products.…”

“…[28]. T-AOC is representative of comprehensive antioxidant enzymes in various tissues of the body, and MDA is commonly used as a biomarker of oxidative stress, which is a lipid oxidation final product [8]. In accordance with previous reports, anomalous changes in the activities of enzymatic and nonenzymatic antioxidants due to D-gal exposure were found in the current study, and our experimental ndings showed that UB intervention could distinctly attenuate the MDA content and antioxidant enzyme activities in mice, which may be one mechanism by which UB improves learning and memory in D-gal-exposed aging mice [9,15].…”

“…Evidence for the presence of a large body of aging models has veri ed that continuous chronic administration of a low dose of D-gal can produce aging-associated AD-like performance, including a disruption of de cits in learning and spatial memory, synaptic damage, neuronal loss, reduced activities of antioxidant enzymes and increased production of ROS [8,9]. Similarly, recent studies have shown that neuronal cell death is caused by a strengthened OS and could exacerbate motor and cognitive behavioral de cits [10].…”