2020
DOI: 10.7150/ijms.38602
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Homocysteine (Hcy) accelerates neuronal senescence and induces age-related neurodegenerative diseases. Silence signal regulating factor 1 (SIRT1) prolongs lifespan and takes neuroprotective effects. We have previously demonstrated that hydrogen sulfide (H2S) prevents Hcy-induced apoptosis of neuronal cells and has neuroprotective effect. In the present work, we aimed to investigate whether H2S protects HT22 cells against Hcy-induced neuronal senescence and whether SIRT1 mediates this role of H2S. We found that… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

1
3
0

Year Published

2020
2020
2023
2023

Publication Types

Select...
8

Relationship

1
7

Authors

Journals

citations
Cited by 12 publications
(4 citation statements)
references
References 59 publications
1
3
0
Order By: Relevance
“…Protective effects of H 2 S upon Hcy overexposure may also involve up-regulation of SIRT1 expression, a key regulator of redox homeostasis, as well as inhibition of ER stress, as evidenced by the down-regulation of GRP78 and cleaved caspase-12 protein expression in PC12 cells [ 85 ]. Similar effects were observed in HT22 cells, being associated with reduced Hcy-induced cellular senescence [ 86 ]. In turn, the up-regulation of BDNF expression and BDNF/TrkB signaling by H 2 S significantly reduced hippocampal ER stress and apoptosis in Hcy-exposed rats [ 87 ], thus preventing cognitive decline in response to Hcy [ 88 ].…”
Section: Endogenous Neurotoxicantssupporting
confidence: 68%
“…Protective effects of H 2 S upon Hcy overexposure may also involve up-regulation of SIRT1 expression, a key regulator of redox homeostasis, as well as inhibition of ER stress, as evidenced by the down-regulation of GRP78 and cleaved caspase-12 protein expression in PC12 cells [ 85 ]. Similar effects were observed in HT22 cells, being associated with reduced Hcy-induced cellular senescence [ 86 ]. In turn, the up-regulation of BDNF expression and BDNF/TrkB signaling by H 2 S significantly reduced hippocampal ER stress and apoptosis in Hcy-exposed rats [ 87 ], thus preventing cognitive decline in response to Hcy [ 88 ].…”
Section: Endogenous Neurotoxicantssupporting
confidence: 68%
“…Performing the surgery at E11.5 also gives a good ‘therapeutic window’. The protective effect of H 2 S has been widely reported in cardiovascular [ [38] , [39] , [40] , [41] ], neurodegenerative diseases [ 42 , 43 ] and in multiple cancer pathophysiology [ [44] , [45] , [46] ]. In this study, we used MZe786, which is a H 2 S releasing aspirin as a source of H 2 S. Chronic use of aspirin is frequently associated with gastropathy, partly due to, redox imbalances [ 47 ].…”
Section: Discussionmentioning
confidence: 99%
“…These studies reveal that SIRT1 plays an important role in antidepressant-like action [12]. Previous literature has shown that H 2 S has an upregulatory effect on SIRT1 in various cells and tissues [17,18], especially in nerve cells [19,20]. Our previous work reveals that H 2 S promotes the expression of SIRT1 in the hippocampus of CRS-treated rats [21].…”
Section: Introductionmentioning
confidence: 93%