Antioxidative potential of Lactobacillus sp. in ameliorating D-galactose-induced aging

Abstract

Aging is a progressive, unalterable physiological degradation process of living organisms, which leads to deterioration of biological function and eventually to senescence. The most prevalent factor responsible for aging is the accumulation of damages resulting from oxidative stress and dysbiosis. D-galactose-induced aging has become a hot topic, and extensive research is being conducted in this area. Published literature has reported that the continuous administration of D-galactose leads to the deterioration of motor and cognitive skills, resembling symptoms of aging. Hence, this procedure is employed as a model for accelerated aging. This review aims to emphasize the effect of D-galactose on various bodily organs and underline the role of the Lactobacillus sp. in the aging process, along with its anti-oxidative potential. A critical consideration to the literature describing animal models that have used the Lactobacillus sp. in amending D-galactose-induced aging is also given. Key points • D-Galactose induces the aging process via decreasing the respiratory chain enzyme activity as well as ATP synthesis, mitochondrial dysfunction, and increased ROS production. • D-Galactose induced aging primarily affects the brain, heart, lung, liver, kidney, and skin. • The anti-oxidative potential of Lactobacillus sp. in improving D-galactose-induced aging in animal models via direct feeding and feeding of Lactobacillus-fermented food.

Impact of de‐branched starch molecules and fatty acid complexes on the attenuation of ageing‐induced cognitive impairment

“…2(e)) and NO (Fig. 2(f)) increased in the MC group compared with the NC group, showing oxidative damage caused by d ‐galactose 15 . In the three intervention groups, levels of T‐SOD and CAT significantly increased, and serum levels of MDA and NO significantly decreased.…”

“…2 compared with the NC group, showing oxidative damage caused by D-galactose. 15 In the three intervention groups, levels of T-SOD and CAT significantly increased, and serum levels of MDA and NO significantly decreased. Oxidant stress caused by overproduction of reactive oxygen species and/or deficiency of antioxidant defenses can induce cellular senescence.…”

Ratiometric Fluorescent Probe for Real-Time Detection of β-Galactosidase Activity in Lysosomes and Its Application in Drug-Induced Senescence Imaging

“…In a short period of time, most of the probe was concentrated in the heart, kidney, and liver regions, and only a minority reached the lesion site. , As shown in Figure b,c, the fluorescence changes of whole body imaging within 5–90 min in specific channels of mice were detected by animal imager to indicate the activity of β-gal. In the green channel (480–530 nm), with the increase of incubation time, the control group had no obvious enhancement, while the brain and muscle parts of the senescence group 1 and 2 had obvious fluorescence enhancement, which proved that the senescence parts of the mice had highly active β-gal. − While in the red channel (580–630 nm), most of the probe was retained in the heart, kidney, and liver regions; therefore, the fluorescence from the red channel in the corresponding areas was clearly visible. Figure d–f shows the fluorescence quantitative values near the right lower limb of the mice (selected areas in Figure b–c) from the green channel and red channel of the control group and experimental groups 1 ( d -galactose) and 2 (HU).…”

“…The experiment constructed a d -galactose-induced senescence mouse model widely used in biological research. Studies have shown that long-term injection and absorption of d -galactose can cause symptoms similar to natural aging. − d -Galactose induces senescence by reducing respiratory chain enzyme activity and ATP synthesis, leading to mitochondrial dysfunction and increasing ROS production . HU is also considered to be a drug that causes senescence and exerts an antimetabolic compound effect by inhibiting ribonucleotide reductase .…”

“…42−44 D-Galactose induces senescence by reducing respiratory chain enzyme activity and ATP synthesis, leading to mitochondrial dysfunction and increasing ROS production. 45 HU is also considered to be a drug that causes senescence and exerts an antimetabolic compound effect by inhibiting ribonucleotide reductase. 35 Therefore, Dgalactose-and HU-induced living mice senescence were used as the model for in vivo imaging.…”