Reduced expression of SIRT1 and SOD-1 and the correlation between these levels in various regions of the brains of patients with Alzheimer's disease

Cao, Kejiang; Dong, Yang-Ting; Xiang, Jie; Xu, Yi; Hong, Wei; Song, Hui; Guan, Zhi‐Zhong

doi:10.1136/jclinpath-2018-205320

Cited by 40 publications

(33 citation statements)

References 47 publications

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“…Accumulating evidence demonstrated that Sirt1 plays an important role for neuroprotection in several models of neurodegenerative diseases, such as Alzheimer's disease (AD) (Fujita and Yamashita, 2018), while the level of hippocampal Sirt1 were significantly decreased in patients with AD (Cao et al, 2018). Meanwhile, it has been demonstrated that oxymatrine attenuated hippocampus ischemia/reperfusion injury through upregulation of Sirt1 (Zhou et al, 2018), indicating that Sirt1 acts as a key factor in hippocampal damage.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Zuo

Jiang

et al. 2020

Front. Neurosci.

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Sleep deprivation (SD) induces hippocampal damage. Hydrogen sulfide (H 2 S) is a neuronal protective factor. Silence information regulating factor 1 (Sirt1) plays an important role in neuroprotection. Therefore, this study was aimed at exploring whether H 2 S meliorates SD-induced hippocampal damage and whether Sirt1 mediates this protective role of H 2 S. We found that sodium hydrosulfide (NaHS, a donor of H 2 S) alleviated SD-generated hippocampal oxidative stress, including increases in the activation of SOD and the level of GSH as well as a decrease in the level of MDA. Meanwhile, we found that NaHS reduced SD-exerted hippocampal endoplasmic reticulum (ER) Stress, including downregulations of GRP78, CHOP, and cleavedcaspase-12 expression. Moreover, NaHS reduced the apoptosis in the SD-exposed hippocampus, and this included decreases in the number of apoptotic cells and the activation of caspase-3, downregulation of Bax expression, and upregulation of Bcl-2 expression. NaHS upregulated the expression of Sirt1 in the hippocampus of SDexposed rats. Furthermore, Sirtinol, the inhibitor of Sirt1, abrogated the protection of NaHS against SD-exerted hippocampal oxidative stress, ER stress, and apoptosis. These results suggested that H 2 S alleviates SD-induced hippocampal damage by upregulation of hippocampal Sirt1.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Zuo

Jiang

et al. 2020

Front. Neurosci.

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“…A decline in normal antioxidant defense mechanisms has been observed in the aging brain and in the case of several neurodegenerative diseases. 19 Such a decline increases the vulnerability of the brain to the deleterious effects of oxidative damage; the brains of patients with Alzheimer's disease showed reduced activity of antioxidant enzymes (SOD, catalase, glutathione peroxidase and glutathione reductase) 26,27. Different markers of oxidative stress in the aging brain have been broadly researched, for example 8-OHdG (8-hydroxy-2′-deoxyguanosine) as a biomarker of oxidative DNA damage in the aged brain [28][29][30].…”

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confidence: 99%

Oxidative stress in elderly population: A prevention screening study

Gorni¹,

Finco²

2020

Aging Medicine

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Aging is characterized by a progressive decline in the efficiency of biochemical and physiological processes, the functional maintenance of tissue homeostasis and an increasing susceptibility to diseases. Aging is a multifactorial process, which is genetically determined and influenced epigenetically by environment. 1 In recent years it has been well known that oxidative stress may play important roles in elderly health and, in particular, there is increasing evidence that aging might be caused by the potential and harmful effects of an accumulation of oxidative damage caused by reactive species (RS, in particular reactive oxygen species or ROS and reactive nitrogen species RNS). This evidence is supported by the "free radical theory of aging" proposed by Harman. 2

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“…A large body of evidence suggests that oxidative stress plays an important part in the pathogenesis of AD (Youssef et al, ). SOD is important antioxidant enzymes protected cellule against damage caused by oxygen‐derived free radicals, by means of removing toxic peroxide metabolites and blocking lipid peroxidation chain reaction (Cao et al, ). The MDA as index of lipid peroxidation has attracted widespread interest, because it appears to offer a means of assessing lipid peroxidation in biological materials (Tian et al, ).…”

Section: Discussionmentioning

confidence: 99%

Kaempferide prevents cognitive decline via attenuation of oxidative stress and enhancement of brain‐derived neurotrophic factor/tropomyosin receptor kinase B/cAMP response element‐binding signaling pathway

Yan

et al. 2019

Phytotherapy Research

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Kaempferide (KF) is a compound of flavonoids from Alpinae oxyphylla Miq, and the herb itself is used as a classical tonic agent. This paper aims to investigate the effects of KF on cognitive function impairment and neurodegeneration in the mouse model of Alzheimer's disease induced by intracerebroventricular (ICV) injection of Aβ 1-42 . The mice were treated with KF at doses of 0.02 and 0.2 mg/kg/day (ICV) for five consecutive days after Aβ 1-42 exposures. The behavioral test results showed that KF could prevent cognitive decline in mice induced by Aβ 1-42 as assessed by the locomotor activity test, Y-maze test, and Morris water maze test.Furthermore, the activities of superoxide dismutase and malondialdehyde in the hippocampus and cerebral cortex were elevated by KF administration. Results of hippocampus slices showed that neurons were integrated and regularly arranged in the groups, which were administered along with KF. In addition, we found KF could boost brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element-binding (CREB) protein signal in the hippocampus.All results illustrated that KF could exert neuroprotective effects at least partly through alleviating oxidative stress and enhancing the BDNF/TrkB/CREB pathway in Aβ 1-42 -induced mice.

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Reduced expression of SIRT1 and SOD-1 and the correlation between these levels in various regions of the brains of patients with Alzheimer's disease

Abstract: These findings indicate that the reduced level of SIRT1 in the brains of patients with AD may be related to the decline in SOD-1 and neuropathological changes of this disorder.

Cited by 40 publications

References 47 publications

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Oxidative stress in elderly population: A prevention screening study

Kaempferide prevents cognitive decline via attenuation of oxidative stress and enhancement of brain‐derived neurotrophic factor/tropomyosin receptor kinase B/cAMP response element‐binding signaling pathway

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