H2S Attenuates Sleep Deprivation-Induced Cognitive Impairment by Reducing Excessive Autophagy via Hippocampal Sirt-1 in WISTAR RATS

Gao, Shan; Tang, Yiyun; Jiang, Li; Lan, Fang; Li, Xiang; Zhang, Ping; Zou, Wei; Chen, Yongjun; Tang, Xiao‐Qing

doi:10.1007/s11064-021-03314-0

Cited by 15 publications

(5 citation statements)

References 57 publications

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“…27 The MWM is widely used to objectively evaluate the spatial memory, and discriminability of animals. 28 The experimental workflow is described in Fig. 1a, and the Brassica rapa L. was identified in Fig.…”

Section: Resultsmentioning

confidence: 99%

Brassica rapa L. (Tibetan turnip) prevents sleep-deprivation induced cognitive deficits via the inhibition of neuroinflammation and mitochondrial depolarization

et al. 2022

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Section: Resultsmentioning

confidence: 99%

Brassica rapa L. (Tibetan turnip) prevents sleep-deprivation induced cognitive deficits via the inhibition of neuroinflammation and mitochondrial depolarization

et al. 2022

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“…Moreover, the expression of these proteins could be regulated by NaHS to ameliorate the myocardial damage. H 2 S attenuated sleep deprivationinduced cognitive impairment by reducing excessive autophagy of hippocampal SIRT 1 in WISTAR rats [30]. H 2 S protected retinal pigment epithelial cells from oxidative stress-induced apoptosis and afected autophagy [31].…”

Section: Discussionmentioning

confidence: 98%

Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced Cardiomyocytes Injury

Jin,

Huang,

et al. 2023

Journal of Toxicology

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Objective. The aim of this study was to investigate the effects of sodium hydrosulfide (NaHS) on Lipopolysaccharide (LPS)-induced cardiomyocyte injury in H9c2 cells. Methods. H9c2 cardiomyocytes cultivated with medium containing 10 μg/mL LPS were used to recapitulate the phenotypes of those in sepsis. Two sequential experiments were performed. The first contained a control group, a LPS group, and a LPS + NaHS group, with the aim to assure the protective effects of NaHS on LPS-treated cardiomyocytes. The second experiment added a fourth group, the LPS + NaHS + miR-133a-3p inhibition group, with the aim to preliminarily explore whether miR-133-3p exerts a protective function downstream of NaHS. The adenosine triphosphate (ATP) kit was used to detect ATP content; real-time quantitative polynucleotide chain reaction (qPCR) was used to measure the levels of mammalian targets of rapamycin (mTOR), AMP-dependent protein kinase (AMPK), and miR-133a-3p, and Western blot (WB) was used to detect protein levels of mTOR, AMPK, myosin-like Bcl2 interacting protein (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3I/II), and P62 (sequestosome-1, sqstm-1/P62). Results. Compared with the control group, the expressions of miR-133a-3p ( P < 0.001), P62 ( P < 0.001), and the content of ATP ( P < 0.001) decreased, while the expressions of Beclin-1 ( P = 0.023) and LC3I/II ( P = 0.048) increased in the LPS group. Compared with the LPS group, the expressions of miR-133a-3p ( P < 0.001), P62 ( P < 0.001), and the content of ATP ( P < 0.001) in the NaHS + LPS group increased, while the expressions of Beclin-1 ( P = 0.023) and LC3I/II ( P = 0.022) decreased. Compared with the NaHS + LPS group, the expression levels of miR-133a-3p ( P < 0.001), P62 ( P = 0.001), and the content of ATP ( P < 0.001) in the LPS + NaHS + miR-133a-3p inhibition group were downregulated, and the expression levels of Beclin-1 ( P = 0.012) and LC3I/II ( P = 0.010) were upregulated. The difference was statistically significant. There was no significant difference in the expression of AMPK and mTOR between groups. Conclusion. Our research demonstrated that NaHS relieved LPS-induced myocardial injury in H9c2 by promoting the expression of miR-133a-3p, inhibiting autophagy in cardiomyocytes, and restoring cellular ATP levels.

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“…Hydrogen sulfide (H 2 S) has been widely acknowledged as a key signaling factor which exhibit positive effects in the management of sleep deprivation. For example, H 2 S was found to antagonize hippocampal damage in sleep-deprived rat models (15), and further alleviate cognitive dysfunction in sleep-deprived rat models by suppressing excessive hippocampal autophagy (16). Moreover, H 2 S could also prevent the depression and anxiety symptoms caused by sleep deprivation by modulating the signaling pathway of silence information regulating factor-1 (Sirt-1), which plays a key role in neuroprotection (17,18) (17,18).…”

Section: P R E P R I N Tmentioning

confidence: 99%

Dietary methionine restriction attenuates cognitive dysfunction associated with sleep deprivation by promoting production of hydrogen sulfide, upregulating expression of BDNF and suppressing neuro-inflammation in rats

Ouyang

Peng

et al. 2023

Arch Med Sci

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IntroductionIn this study, we aimed to study the potential role of H2S and the application of dietary methionine restriction (DMR) in the treatment of cognitive dysfunction in sleep deprived rat models.Material and methodsThe rat groups were established as a Control group, a sleep deprivation (SD) group, a SD + NaSH group and a SD + DMR group. Behavioral data was studied via Morris water maze test. TUNEL assay, real-time PCR, immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA) were performed to study the differences of cognitive impairment related genes and proteins in different rat groups.ResultsPath length and escape latency were higher in the sleep deprived rats compared with the control rats, which were subsequently recovered by the treatment of NaSH or DMR. Also, DMR most significantly recovered the cognitive impairment and neuron status of sleep deprived rats compared with the administration of NaSH. The elevated level of hippocampal Iba1 and H2S production was recovered by NaSH and DMR, and the expressions of hippocampal phenotypic-related genes including NOS, CD68, CD32 and CD206 mRNA also showed similar trend as hippocampal Iba1. Meanwhile, the increased relative expression of IL-6 and IL-4 were recovered by DMR in sleep deprived rats, while the reduced level of hippocampal brain-derived neurotrophic factor (BDNF) and cystathionine γ-lyase (CSE) were elevated by the treatment of NaSH and MDR, with MDR exhibiting the most significant effect.ConclusionsThe application of DMR could attenuate cognitive dysfunction in sleep deprivation rats by upregulating the production of H2S and BDNF expression and alleviating neuro-inflammation responses.

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H2S Attenuates Sleep Deprivation-Induced Cognitive Impairment by Reducing Excessive Autophagy via Hippocampal Sirt-1 in WISTAR RATS

Cited by 15 publications

References 57 publications

Brassica rapa L. (Tibetan turnip) prevents sleep-deprivation induced cognitive deficits via the inhibition of neuroinflammation and mitochondrial depolarization

Brassica rapa L. (Tibetan turnip) prevents sleep-deprivation induced cognitive deficits via the inhibition of neuroinflammation and mitochondrial depolarization

Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced Cardiomyocytes Injury

Dietary methionine restriction attenuates cognitive dysfunction associated with sleep deprivation by promoting production of hydrogen sulfide, upregulating expression of BDNF and suppressing neuro-inflammation in rats

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