Advanced glycation in d-galactose induced mouse aging model

Xu, Shu; Bao, Mingmin; Li, Dian-Dong; Li, Yong Ming

doi:10.1016/s0047-6374(99)00022-6

Cited by 360 publications

(286 citation statements)

References 22 publications

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“…The aging model shows neurological impairment, decreased activity of antioxidant enzymes and poor immune responses. D-Galactose is a reducing sugar that can form advanced glycation end products in vivo, which can not be further metabolized and accumulate in nerve cells; this effect at least partially contributes to the pathological mechanism of this aging model (Song et al, 1999). Therefore, D-galactose-treated mice were used as an experimental senile model to investigate the antiaging effect of CSE.…”

Section: Discussionmentioning

confidence: 99%

Antiaging effect of Cordyceps sinensis extract

Jia

et al. 2008

Phytotherapy Research

104

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This experiment studied the effect of Cordyceps sinensis extract (CSE) on mice aged by D-galactose and castrated rats to analyse its antiaging effect. Water maze and step-down type avoidance tests were used to examine the effect of CSE on learning and memory. CSE shortened escape latency, prolonged step-down latency and decreased the number of errors in mice aged by D-galactose. The effect of CSE on the sexual function of castrated rats was evaluated by measuring the penis erection latency, mount latency and ejaculation latency. CSE appeared to shorten penis erection latency and mount latency in castrated rats. The study also measured the effect of CSE on the activity of age-related enzymes. The results showed that CSE improved the activity of superoxide dismutase, glutathione peroxidase and catalase and lowered the level of lipid peroxidation and monoamine oxidase activity in the aged mice. The study demonstrated that CSE can improve the brain function and antioxidative enzyme activity in mice with D-galactose-induced senescence and promote sexual function in castrated rats. All of these findings suggest that CSE has an antiaging effect.

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Section: Discussionmentioning

confidence: 99%

Antiaging effect of Cordyceps sinensis extract

Jia

et al. 2008

Phytotherapy Research

104

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“…5, 6) immunoreactivity was detected in the mice subjected to combined D-gal and Al treatment. and error rate in behavioral tests, and increased skin hydroxyproline content [11] . Furthermore, these mice show significant decreases in motor activity, lymphocyte mito- Previous research showed that AD brains contain increased levels of Al.…”

Section: Combined Administration Of D-gal and Al For 8 And 10mentioning

confidence: 93%

Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

et al. 2011

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“…Rodent chronic administration of D-galactose has been used as an animal model in aging research (31). We also monitored phosphorylation and sulfhydration of p66Shc in D-galactose-induced cellular and animal senescent models.…”

Section: Effect Of H 2 S On Oxidative Stress-induced Senescencementioning

confidence: 99%

Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide

Xie

Shi²,

Xie³

et al. 2014

Antioxidants & Redox Signaling

116

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Aims: Mitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H 2 S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H 2 S is mediated by p66Shc. Results: Application of exogenous H 2 S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine b-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H 2 O 2 /D-galactose in SH-SY5Y cells or in the mice cortex. H 2 S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKC bII and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H 2 S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H 2 S. Innovation: We revealed a novel mechanism for the antioxidant effect of H 2 S and its role in oxidative stress-related diseases. Conclusion: H 2 S inhibits mitochondrial ROS production via the sulfhydration of Cys-59 residue, which in turn, prevents the phosphorylation of p66Shc. Antioxid. Redox Signal. 21, 2531-2542.

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Advanced glycation in d-galactose induced mouse aging model

Cited by 360 publications

References 22 publications

Antiaging effect of Cordyceps sinensis extract

Antiaging effect of Cordyceps sinensis extract

Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide

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