Comparison of behavioral and biochemical deficits in rats with hereditary defined or d-galactose-induced accelerated senescence: Evaluating the protective effects of diosgenin

Tikhonova, Maria A.; Yu, Ching‐Han; Kolosova, N. G.; Gerlinskaya, L. A.; Maslennikova, Svetlana; Yudina, Alexandra V.; Amstislavskaya, Tamara G.; Ho, Ying-Jui

doi:10.1016/j.pbb.2014.01.012

Cited by 26 publications

(18 citation statements)

References 60 publications

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“…Also, defecation and urination in the open field and plus-maze was similar in all groups of rats, showing similar emotionality during the experiment. These results corroborate previous studies 12,18,20 that did not find alterations in the exploratory locomotor activity and anxiety levels in the openfield test associated with d-galactose treatment.…”

Section: Discussionsupporting

confidence: 92%

“…18,20 On the contrary, there are several studies 12,14,23,62 that reported impairments of the spatial learning and memory induced by d-galactose treatment. Indeed, in a study where C57BL/6 mice were used, there were deficits in spatial learning and memory but curiously, non-spatial cognitive ability such as novelty-seeking behavior was not affected.…”

Section: Discussionmentioning

confidence: 99%

“…injection of 150 mg/kg per day) did not affect sexual incentive motivation, working memory, and object recognition in Wistar male rats. 20 Likewise, Salkovic-Petresic and collaborators found that 1-month oral galactose treatment (200 mg/kg per day) failed to induce changes in the spatial memory of male Fisher and female Wistar rats. 19 Several factors could be at the base of the apparent lack of congruence of d-galactose as an accelerated aging model.…”

Section: Introductionmentioning

confidence: 98%

“…16,17 It is important to note that, more recently, some dissonant reports concerning the effectiveness of this accelerated aging paradigm have been published. [18][19][20] Indeed, Parameshwaran and collaborators have concluded that the d-galactose treatment (intraperitoneal [i.p] injection of 100 mg/kg per day) in female C57BL/61 mice was not suitable for testing antioxidant compounds in mice. 18 Moreover, Tikhonova and collaborators found that d-galactose treatment (i.p.…”

Section: Introductionmentioning

confidence: 99%

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d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Cardoso

Magano

Marrana

et al. 2015

Rejuvenation Research

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The model of accelerated senescence with the prolonged administration of d-galactose is used in anti-aging studies because it mimics several aging-associated alterations such as increase of oxidative stress and decline of cognition. However, there is no standardized protocol for this aging model, and recently some reports have questioned its effectiveness. To clarify this issue, we used a model of high-dose d-galactose on 1-month-old male Wistar rats and studied the hippocampus, one of the most affected brain regions. In one group (n = 10), d-galactose was daily administered intraperitoneally (300 mg/kg) during 8 weeks whereas age-matched controls (n = 10) were injected intraperitoneally with saline. A third group (n = 10) was treated with the same dose of d-galactose and with oral epigallocatechin-3-gallate (EGCG) (2 grams/L), a green tea catechin with anti-oxidant and neuroprotective properties. After treatments, animals were submitted to open-field, elevated plus-maze and Morris water maze tests, and neurogenesis in the dentate gyrus subgranular layer was quantified. There were no significant alterations when the three groups were compared in the number of doublecortin-and Ki-67-immunoreactive cells, and also on anxiety levels, spatial learning, and memory. Therefore, d-galactose was not effective in the induction of accelerated aging, and EGCG administered to d-galactose-treated animals did not improve behavior and had no effects on neurogenesis. We conclude that daily 300 mg/kg of d-galactose administered intraperitoneally may not be a suitable model for inducing age-related neurobehavioral alterations in young male Wistar rats. More studies are necessary to obtain a reliable and reproducible model of accelerated senescence in rodents using d-galactose.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Cardoso

Magano

Marrana

et al. 2015

Rejuvenation Research

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show abstract

“…The latter may evidence compensatory mechanisms that explain the absence of significant changes in olfactory function. Interestingly, earlier we found the decreased sexual motivation in 5-months old OXYS males [39]. The present findings suggested that olfactory dysfunction was not involved in the disturbances of sexual behavior in OXYS males.…”

Section: Discussionsupporting

confidence: 49%

Comparative study of perception and processing of socially or sexually significant odor information in male rats with normal or accelerated senescence using fMRI

Tikhonova

Romaschenko

Akulov

et al. 2015

Behavioural Brain Research

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Diosgenin protects retinal pigment epithelial cells from inflammatory damage and oxidative stress induced by high glucose by activating AMPK/Nrf2/HO‐1 pathway

Yang

Gao

2022

Immunity Inflam & Disease

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Introduction Diosgenin is a natural steroidal compound with reported antidiabetic and many other protective properties. This study aimed to explore the protective effect of diosgenin on high‐glucose (HG)‐induced retinal pigment epithelial cells. Methods HG‐induced ARPE‐19 cells were considered as a cell model of diabetic retinopathy (DR). The viability and apoptosis of ARPE‐19 cells induced by HG treated with either diosgenin or Compound C (CC; dorsomorphin) were detected by Cell Counting Kit‐8 assay and flow cytometric analysis. The expression of apoptosis‐related proteins, inflammation‐related proteins, and AMPK/Nrf2/HO‐1 pathway‐related proteins was detected by western blotting. The levels of inflammatory cytokines and detection of oxidative stress indexes were performed using the appropriate assay kits. The messenger RNA expression of inflammatory cytokines was detected by real‐time quantitative polymerase chain reaction. Results There was no obvious effect of diosgenin on the viability of ARPE‐19 cells and the viability of ARPE‐19 cells was significantly reduced after HG induction. However, diosgenin increased the viability, inhibited the apoptosis, and reduced the inflammatory response and oxidative stress of ARPE‐19 cells induced by HG. In addition, diosgenin could activate the AMPK/Nrf2/HO‐1 pathway. CC, an AMPK inhibitor, could reverse the above changes caused by diosgenin treatment in ARPE‐19 cells induced by HG. Conclusions Diosgenin could protect ARPE‐19 cells from inflammatory damage and oxidative stress induced by HG, by activating the AMPK/Nrf2/HO‐1 pathway.

show abstract

Comparison of behavioral and biochemical deficits in rats with hereditary defined or d-galactose-induced accelerated senescence: Evaluating the protective effects of diosgenin

Cited by 26 publications

References 60 publications

d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

d-Galactose High-Dose Administration Failed to Induce Accelerated Aging Changes in Neurogenesis, Anxiety, and Spatial Memory on Young Male Wistar Rats

Comparative study of perception and processing of socially or sexually significant odor information in male rats with normal or accelerated senescence using fMRI

Diosgenin protects retinal pigment epithelial cells from inflammatory damage and oxidative stress induced by high glucose by activating AMPK/Nrf2/HO‐1 pathway

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