Sirt1 Mediates Improvement in Cognitive Defects Induced by Focal Cerebral Ischemia Following Hyperbaric Oxygen Preconditioning in Rats

Ding, Philip Yu‐An; Ren, Daoyuan; He, Shuang; He, Manman; Zhang, G; Chen, Y; Sang, Hanfei; Peng, Zhengwu; Yan, Wenjun

doi:10.33549/physiolres.933544

Cited by 12 publications

(7 citation statements)

References 63 publications

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“…Furthermore, SRT1720 upregulated GSH-PX, GSH and SOD levels, and downregulated levels of MDA, in DM rats. Consistent with the findings of the present study, Ding et al (12) reported that improvements observed in rat cognitive deficits following hyperbaric oxygen preconditioning was mediated by SIRT1. These results demonstrate that SRT1720 may have potential as a novel drug for cognitive impairment in diabetes.…”

Section: Discussionsupporting

confidence: 93%

A SIRT1 agonist reduces cognitive decline in type 2 diabetic rats through antioxidative and anti‑inflammatory mechanisms

et al. 2018

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Sirtuin 1 (SIRT1) is an NAD+-dependent protein deacetylase that is involved in cell differentiation, aging, apoptosis, physiological rhythms, metabolic regulation, oxidative stress and numerous other important biological processes. In the present study, the ability of a sirtuin-1 (SIRT1) agonist, SRT1720, to reduce cognitive decline in type 2 diabetes mellitus (T2DM) was investigated. Streptozotocin-induced male Sprague-Dawley rats were used to establish a T2DM model and the protective effect of SRT1720 and its underlying mechanisms were investigated. Body weight and fasting blood glucose (FBG) were recorded and cognitive function was measured with the Morris water maze. Levels of oxidative stress, inflammation, caspase-3 activity and nuclear factor κB (NF-κB) mRNA expression were detected with a series of commercial assay kits and reverse transcription-quantitative polymerase chain reaction, respectively. Western blot analysis was performed to determine the protein expression of NF-κB, endothelial nitric oxide synthase (eNOS), peroxisome proliferator-activated receptor γ (PPARγ), AMP-activated protein kinase (AMPK), heat shock 70 kDa protein (HSP70), SIRT1, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1). The results revealed that SRT1720 significantly increased body weight, decreased FBG, improved cognitive function and reduced the levels of proteins associated with oxidative stress and inflammation damage in T2DM rats. Additionally, SRT1720 significantly decreased NF-κB p65 mRNA expression and increased eNOS and PPARγ expression. SRT1720 significantly reduced caspase-3 activity and HSP70 protein expression, and increased p-AMPK, SIRT1, Nrf2 and HO-1 protein expression. Collectively, the results indicate that SRT1720 may reduce cognitive decline in T2DM rats through antioxidative and anti-inflammatory action via NF-κB and AMPK-dependent mechanisms.

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Section: Discussionsupporting

confidence: 93%

A SIRT1 agonist reduces cognitive decline in type 2 diabetic rats through antioxidative and anti‑inflammatory mechanisms

et al. 2018

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“…The number of HBO sessions used in clinical medicine has not been firmly standardized as it substantially depends on the given medical condition; it could range from several to 60 sessions (Mathieu et al 2017). In animal experiments, the number of HBO exposures usually ranges between 1 and 15 (Ay et al 2007, Ding et al 2017, Limirio et al 2018, Sun et al 2017; studies on HBO impact on ex vivo models using various cell types usually report from 1 to 7 HBO exposures (Kang et al 2004) and document that the effect of treatment is detectable even after a single exposure. For our experiments we have thus selected conditions mimicking chronic HBO treatment on the cellular model.…”

Section: Discussionmentioning

confidence: 99%

Repeated Exposure to Hyperbaric Hyperoxia Affects Mitochondrial Functions of the Lung Fibroblasts

Dejmek

Kohoutová²,

Kripnerová³

et al. 2018

Physiol Res

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Hyperbaric oxygen (HBO) therapy, i.e. breathing pure oxygen under increased environmental pressures serves as a treatment for diverse medical conditions. However, elevated oxygen concentration can be detrimental to central nervous system or lungs. Our study aimed to evaluate the effects of repeated exposure to HBO on mitochondrial respiration assessed by high-resolution respirometry (HRR), cell viability estimated by PrestoBlue® reaction, morphology analyzed by routine phase contrast and fluorescent microscopy, and superoxide dismutase (SOD) and citrate synthase (CS) activities using human lung fibroblasts. The cells were exposed to HBO for 2 h per day for 5 consecutive days. One day after the last exposure, HBO cells displayed significantly smaller area and perimeter, compromised viability and elevated SOD activity. No changes were detected in CS activity or quality of mitochondrial network. HRR revealed impaired mitochondrial oxygen consumption manifested by increased leak respiration, decreased activity of complex II and compromised ATP-related oxygen consumption when fatty acids were oxidized. Our findings document that in conditions mimicking chronic intermittent exposure to HBO, lung fibroblasts suffer from compromised mitochondrial respiration linked to complex II and impaired cellular growth in spite of increased antioxidant defense. Underlying mechanism of this HBO-induced mitochondrial dysfunction should be further explored.

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“…Activating or inhibiting the SIRT1 enzymatic activity results in a decrease or an increase in infarct volume ( Zhang, Zhang, & Wu, 2018 ). As an example, Ding et al pointed out that hyperbaric oxygen preconditioning increased phosphorylated neurofilament heavy polypeptides and doublecortin in the hippocampus as well as mitigated cognitive deficits in MCAO/R rats, but these effects were abolished by the SIRT1 knockdown ( Ding et al, 2017 ). Of note, in our study, the expression of SIRT1 was decreased drastically in OGD/R–induced hippocampal cells and MCAO/R–induced brain tissues.…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A and Anhydrosafflor Yellow B Protect Against Cerebral Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Apoptosis via the Silent Information Regulator 1 Signaling Pathway

et al. 2021

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Hydroxysafflor yellow A (HSYA) and anhydrosafflor yellow B (AHSYB) are the main water-soluble compounds in Carthamus tinctorius L. However, studies on the effect of AHSYB on cerebral ischemia/reperfusion (I/R) injury and the therapeutic effect of HSYA by regulating silent information regulator 1 (SIRT1) pathway remain obscure. In this study, we investigated whether the neuroprotective effects of HSYA and AHSYB on oxygen-glucose deprivation/reoxygenation in primary-cultured hippocampal neuronal cells and the middle cerebral artery occlusion and reperfusion model in rats are associated with the regulation of the SIRT1 pathway. In vitro, HSYA and AHSYB increased cell viability, depressed oxidation properties, and reduced neuronal cell apoptosis. In vivo results showed that HSYA and AHSYB effectively reduced infarct volume, improved neurological function, suppressed apoptosis, and decreased the oxidative stress reaction. Besides, RT-PCR and Western blot analysis showed that HSYA and AHSYB increased the mRNA and protein expressions of the main factors in the SIRT1 pathway, including SIRT1, forkhead box O (FOXO) 1, and peroxisome proliferator–activated receptor coactivator 1α (PGC1α), decreased the expression of Bax, and increased the expression of Bcl-2. The results from immunohistochemistry also showed that the expressions of SIRT1, FOXO1, and PGC1α were increased after treatment with HSYA and AHSYB. Furthermore, the neuroprotective effects of HSYA and AHSYB were abolished by EX527 (SIRT1–specific inhibitor). These results indicated that HSYA and AHSYB should be developed into potential drugs for treating cerebral I/R injury via the SIRT1 pathway. Although HSYA and AHSYB have different chemical structures, both of them exert similar neuroprotective properties against I/R injury in vitro and in vivo, which means that AHSYB is also a non-negligible component in safflower.

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Sirt1 Mediates Improvement in Cognitive Defects Induced by Focal Cerebral Ischemia Following Hyperbaric Oxygen Preconditioning in Rats

Cited by 12 publications

References 63 publications

A SIRT1 agonist reduces cognitive decline in type 2 diabetic rats through antioxidative and anti‑inflammatory mechanisms

A SIRT1 agonist reduces cognitive decline in type 2 diabetic rats through antioxidative and anti‑inflammatory mechanisms

Repeated Exposure to Hyperbaric Hyperoxia Affects Mitochondrial Functions of the Lung Fibroblasts

Hydroxysafflor Yellow A and Anhydrosafflor Yellow B Protect Against Cerebral Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Apoptosis via the Silent Information Regulator 1 Signaling Pathway

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