Hydrogen Sulfide Ameliorates Homocysteine-Induced Cognitive Dysfunction by Inhibition of Reactive Aldehydes Involving Upregulation of ALDH2

Li, Min; Zhang, Ping; Wei, Hou; Li, Manhong; Zou, Wei; Li, Xiang; Gu, Hong‐Feng; Tang, Xiao‐Qing

doi:10.1093/ijnp/pyw103

Cited by 28 publications

(28 citation statements)

References 70 publications

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“…Our previous studies have demonstrated that H 2 S has a protective effect against Hcy-evoked neurotoxicity [20,[24][25][26]. Considering the cellular senescence is prominent in the neurotoxicity of Hcy [3,[27][28][29], the present work was designed to explore whether the protection of H2S against the neurotoxicity of Hcy is associated with regulating neuronal senescence.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of SIRT1

Kang¹,

Li²,

Xie³

et al. 2020

Int. J. Med. Sci.

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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 Hcy induced cellular senescence in HT22 cells, as determined by β-galactosidase staining, expressions of P16 INK4a , P21 CIPL , and trypan blue Staining, which are the markers of cellular senescence. However, sodium hydrosulfide (NaHS, the donor of H2S) significantly reversed Hcy-induced cellular senescence. Interestingly, NaHS not only up-regulated the expression of SIRT1 in HT22 cells but also reversed Hcy-downregulated the expression of SIRT1 in HT22 cells. Furthermore, we found that pretreatment with Sirtinol (an inhibitor of SIRT1) markedly reversed the protection of NaHS against Hcy-induced HT22 cells senescence and apoptosis. Our findings illustrated that H2S protects HT22 cells against Hcy-induced senescence by up-regulating SIRT1.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of SIRT1

Kang¹,

Li²,

Xie³

et al. 2020

Int. J. Med. Sci.

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“…Sniffing and touching of the objects (distance within 1 cm) were considered exploratory behaviors, whilst climbing on the objects or chewing were not. Discrimination index, which was calculated as the time difference between new and familiar object exploration/total time, was adopted to evaluate animal cognitive function (21,22). Y-maze test.…”

Section: Animalsmentioning

confidence: 99%

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Yuan

Huang

et al. 2020

Exp Ther Med

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Acute liver failure (ALF) is a devastating clinical syndrome with a high mortality rate if not treated promptly. Previous studies have demonstrated the beneficial effects of hydrogen sulfide (H 2 S) on the brain and liver. The present study aimed to investigate the potential protective effects of H 2 S in ALF. A mouse model of ALF was established following treatment with thioacetamide (TAA). Mice with TAA-induced ALF were intraperitoneally injected with 30 or 100 µmol/kg/day sodium hydrosulfide (NaHS; a H 2 S donor drug) for two weeks. According to results from novel object recognition and Y-maze tests, in the present study, NaHS treatment alleviated cognitive deficiency and preserved spatial orientation learning ability in TAA-induced ALF mice compared with those of untreated mice. In addition, NaHS treatment reduced serum levels of aspartate transaminase (AST), alanine transaminase (ALT) and the concentration of ammonia compared with those that received control treatment, resulting in weight loss prevention. These findings suggested a beneficial effect of H 2 S on liver function. In conclusion, results from the present study suggested that H 2 S treatment may alleviate cognitive deficiency and hepatic dysfunction in mice with ALF, indicating the potential therapeutic benefits of applying H 2 S for the treatment of ALF.

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“…Accumulating evidences demonstrate that H 2 S facilitates the induction of hippocampal long term potentiation (LTP) [ 8 , 9 ] and attenuates hepatic I/R- or β-amyloid-induced impairment in spatial learning and memory [ 10 - 13 ]. Moreover, our recent study certified that disturbance of endogenous H 2 S generation in hippocampus is involved in deficits in learning and memory [ 14 , 15 ] and that H 2 S antagonizes formalydehyde-exerted deficits in cognitive function [ 16 ]. Thus, the present work was to explore whether H 2 S ameliorates CRS-induced cognitive impairment.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide attenuates chronic restrain stress-induced cognitive impairment by upreglulation of Sirt1 in hippocampus

Chen

Luo

et al. 2017

Oncotarget

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Chronic restraint stress (CRS) has detrimental effects on cognitive function. Hydrogen sulfide (H2S), as a neuromodulator, regulates learning and memory. Hippocampus is a key structure in learning and memory. Sirt1 (silence signal regulating factor 1) plays an important role in modulating cognitive function. Therefore, our present work was to investigate whether H2S meliorates CRS-induced damage in hippocampus and impairment in cognition, and further to explore whether the underlying mechanism is via upreglulating Sirt1. In our present work, the behavior experiments [Y-maze test, Novel object recognition (NOR) test, Morris water maze (MWM) test] showed that sodium hydrosulfide (NaHS, a donor of H2S) blocked CRS-induced cognitive impairments in rats. NaHS inhibited CRS-induced hippocampal oxidative stress as evidenced by decrease in MDA level as well as increases in GSH content and SOD activity. NaHS rescued CRS-generated ER stress as evidenced by downregulations of CPR78, CHOP, and cleaved caspase-12. NaHS reduced CRS-exerted apoptosis as evidenced by decreases in the number of TUNEL-positive cells and Bax expression as well as increase in Bcl-2 expression. NaHS upregulated the expression of Sirt1 in the hippocampus of CRS-exposed rats. Furthermore, inhibited Sirt1 by Sirtinol reversed the protective effects of NaHS against CRS-produced cognitive dysfunction and oxidative stress, ER stress as well as apoptosis in hippocampus. Together, these results suggest that H2S meliorates CRS-induced hippocampal damage and cognitive impairment by upregulation of hippocampal Sirt1.

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Hydrogen Sulfide Ameliorates Homocysteine-Induced Cognitive Dysfunction by Inhibition of Reactive Aldehydes Involving Upregulation of ALDH2

Cited by 28 publications

References 70 publications

Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of SIRT1

Hydrogen Sulfide Inhibits Homocysteine-Induced Neuronal Senescence by Up-Regulation of SIRT1

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Hydrogen sulfide attenuates chronic restrain stress-induced cognitive impairment by upreglulation of Sirt1 in hippocampus

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