Salidroside ameliorates cognitive impairment in a d-galactose-induced rat model of Alzheimer’s disease

Gao, Jin; He, He; Jiang, Wenkai; Chang, Xiayun; Zhu, Lingpeng; Luo, Fen; Zhou, Rui; Ma, Chi; Yan, Tianhua

doi:10.1016/j.bbr.2015.06.045

Cited by 131 publications

(62 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As far as we know, this is the first evidence for Sal play an important protective role in neurons through up-regulatingGSK-3β phosphorylation in transgenic flies. As Sal was reported with property of non-toxic and mitigated neurotoxicity [38], our study provides a potential promising drug candidate for AD therapy.…”

Section: Discussionsupporting

confidence: 52%

Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease

Zhang

Chu

et al. 2016

Transl Neurodegener

View full text Add to dashboard Cite

BackgroundAlzheimer’s disease (AD) is an age-related and progressive neurodegenerative disease that causes substantial public health care burdens. Intensive efforts have been made to find effective and safe treatment against AD. Salidroside (Sal) is the main effective component of Rhodiola rosea L., which has several pharmacological activities.The objective of this study was to investigate the efficacy of Sal in the treatment of AD transgenic Drosophila and the associated mechanisms.MethodsWe used tau transgenic Drosophila line (TAU) in which tau protein is expressed in the central nervous system and eyes by the Gal4/UAS system. After feeding flies with Sal, the lifespan and locomotor activity were recorded. We further examined the appearance of vacuoles in the mushroom body using immunohistochemistry, and detected the levels of total glycogen synthase kinase 3β (t-GSK-3β), phosphorylated GSK-3β (p-GSK-3β), t-tau and p-tau in the brain by western blot analysis.ResultsOur results showed that the longevity was improved in salidroside-fed Drosophila groups as well as the locomotor activity. We also observed less vacuoles in the mushroom body, upregulated level of p-GSK-3β and downregulated p-tau following Sal treatment.ConclusionOur data presented the evidence that Sal was capable of reducing the neurodegeneration in tau transgenic Drosophila and inhibiting neuronal loss. The neuroprotective effects of Sal were associated with its up-regulation of the p-GSK-3β and down-regulation of the p-tau.

show abstract

Section: Discussionsupporting

confidence: 52%

Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease

Zhang

Chu

et al. 2016

Transl Neurodegener

View full text Add to dashboard Cite

show abstract

“…Trx was shown to be critically important in protecting C. elegans and SH-SY5Y cells in the dopamine model of Parkinson’s disease [51], and was decreased in the galactose model of Alzheimer’s disease [52]. The cellular content of Trx was also decreased in Alzheimer’s patients, presenting a strong correlation with disease severity and therefore considered a good predictor for the conversion of mild cognitive impairment to Alzheimer’s disease [14].…”

Section: Discussionmentioning

confidence: 99%

Methylglyoxal-induced AMPK activation leads to autophagic degradation of thioredoxin 1 and glyoxalase 2 in HT22 nerve cells

Dafre

Schmitz

Maher

2017

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Methylglyoxal (MGO) is a major glycating agent that reacts with basic residues of proteins and promotes the formation of advanced glycation end products which are believed to play key roles in a number of pathologies, such as diabetes, Alzheimer’s disease, and inflammation. We previously showed that MGO treatment targets the thioredoxin and the glyoxalase systems, leading to a decrease in Trx1 and Glo2 proteins in immortalized mouse hippocampal HT22 nerve cells. Here, we propose that autophagy is the underlying mechanism leading to Glo2 and Trx1 loss induced by MGO. The autophagic markers p62, and the lipidated and active form of LC3, were increased by MGO (0.5 mM). Autophagy inhibition with bafilomycin or chloroquine prevented the decrease in Trx1 and Glo2 at 6 and 18 h after MGO treatment. Proteasome inhibition by MG132 exacerbated the effect of MGO on Trx1 and Glo2 degradation (18 h), further suggesting a role for autophagy. ATG5 small interfering RNA protected Trx1 and Glo2 from MGO-induced degradation, confirming Trx1 and Glo2 loss is mediated by autophagy. In the search for the signals that control autophagy, we found that AMPK activation, a known autophagy inducer, was markedly increased by MGO treatment. AMPK activation was confirmed by increased acetyl coenzyme A carboxylase phosphorylation, a direct AMPK substrate and by decreased mTOR phosphorylation, an indirect marker of AMPK activation. To confirm that MGO-mediated Trx1 and Glo2 degradation was AMPK-dependent, AMPK-deficient mouse embryonic fibroblasts (MEFs) were treated with MGO. Wildtype MEFs presented the expected decrease in Trx1 and Glo2, while MGO was ineffective in decreasing these proteins in AMPK-deficient cells. Overall, the data indicate that MGO activates autophagy in an AMPK-dependent manner, and that autophagy was responsible for Trx1 and Glo2 degradation, confirming that Trx1 and Glo2 are molecular targets of MGO.

show abstract

“…Emerging evidences from clinical and preclinical studies are suggesting that the inhibition of cytokine productions can result in a reduction of inflammation-induced depressive-like behavior (27). The concentrations of proinflammatory cytokines, including IL-6, IL-1b, and TNF-a, were measured in serum and in LPS-treated BV2 microglia cells since they played critical roles in the modulation of emotional behavior (28). The obtained data suggested that the levels of IL-6, IL-1b, and TNF-a were elevated in different degrees in UCMS-induced mice and LPS-induced BV2 cells.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Umbelliferone reverses depression-like behavior in chronic unpredictable mild stress-induced mice via RIP140/NF-κB pathway

Kong

Long

et al. 2016

IUBMB Life

View full text Add to dashboard Cite

show abstract

Salidroside ameliorates cognitive impairment in a d-galactose-induced rat model of Alzheimer’s disease

Cited by 131 publications

References 28 publications

Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease

Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenic Drosophila model of Alzheimer’s disease

Methylglyoxal-induced AMPK activation leads to autophagic degradation of thioredoxin 1 and glyoxalase 2 in HT22 nerve cells

Retracted: Umbelliferone reverses depression-like behavior in chronic unpredictable mild stress-induced mice via RIP140/NF-κB pathway

Contact Info

Product

Resources

About