Dammarane Sapogenins Ameliorates Neurocognitive Functional Impairment Induced by Simulated Long-Duration Spaceflight

Wu, Xiaorui; Dong, Li; Liu, Junlian; Diao, Lihong; Ling, Shukuan; Li, Yuheng; Gao, Jianyi; Fan, Quan-chun; Sun, Wei; Li, Qi; Zhao, Di; Zhong, Guangming; Cao, Dengchao; Liu, Min; Wang, Jiaping; Zhao, Shuang; Liu, Yu; Bai, Guie; Shi, Hongzhi; Xu, Zi; Wang, Jing; Xue, Chunmei; Jin, Xiaoyan; Yuan, Xinxin; Li, Hongxing; Liu, Caizhi; Sun, Huiyuan; Li, Jianwei; Li, Yongzhi; Li, Yingxian

doi:10.3389/fphar.2017.00315

Cited by 45 publications

(35 citation statements)

References 75 publications

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“…Furthermore, our previous study found that GE improved the cognitive performance of scopolamine‐treated mice in the OLR test, which were similar to the present results (Lu, Wang, Lv, et al, ). Thereafter, the MWM task was carried out to evaluate long‐term, spatial learning and memory, which required the rodents to remember and locate a submerged escape platform according to the distal cues (Wu et al, ). Consistent with the previous reports (Lu, Wang, Lv, et al, ; Lu, Wang, Xu, et al, ), after 14‐days CSD, mice showed the prolonged escape latency in the acquisition phase and the decreased crossing number in the probe phase, whereas treatment with GE displayed the improved cognitive performance of CSD‐treated mice in MWM, indicating that it reversed the long‐term, spatial learning and memory dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, our previous study found that GE improved the cognitive performance of scopolamine-treated mice in the OLR test, which were similar to the present results (Lu, Wang, Lv, et al, 2018). Thereafter, the MWM task was carried out to evaluate long-term, spatial learning and memory, which required the rodents to remember and locate a submerged escape platform according to the distal cues (Wu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of Genistein on the cognitive deficits induced by chronic sleep deprivation

Lü

Jiang

et al. 2020

Phytotherapy Research

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Sleep deprivation has been widely reported to cause cognitive dysfunction, and elevation in oxidative stress and inflammation in the body, including the brain, have been suggested as the main factors. Genistein (GE) is an isoflavone widely present in leguminous plants, and it was found to exert a wide spectrum of biological activities, including antioxidant, anti‐inflammatory, hepatoprotective, neuroprotective, and antimetastatic effects. In this study, the protective effect of GE on chronic sleep deprivation (CSD)‐induced cognitive dysfunction was investigated. The mice were subjected to the sleep interruption apparatus and continuously sleep deprived for 25 days. GE was orally administrated (10, 20, and 40 mg/kg) during the sleep deprivation process totally for 25 days. Cognitive behavioral tests were conducted to study the learning and memory using the object location recognition (OLR) task, novel object recognition (NOR) test, and the Morris water maze (MWM) task. Additionally, the cortex and hippocampus were dissected to measure the oxidative stress markers and the antioxidant element nuclear erythroid‐2‐related factor 2 (Nrf2) and its downstream targets, including glutamate cysteine ligase catalytic, glutamate cysteine ligase modifier, heme oxygenase 1, and quinone oxidoreductase 1, as well as nuclear factor kappa B (NF‐κB) p65, nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX‐2) protein expression. Moreover, the pro‐inflammatory cytokines (TNF‐α, interleukin [IL]‐6, and IL‐1β) level was examined in the serum. The current results showed that GE could dose‐dependently ameliorate the cognitive deficits of CSD‐treated mice in the OLR, NOR, and MWM tasks. In addition, GE treatment significantly elevated the activities of total antioxidant capacity and superoxide dismutase and the level of glutathione and lowered the content of malondialdehyde in the cortex and hippocampus of CSD‐treated mice. Furthermore, GE administration effectively activated the antioxidant element Nrf2 and its downstream targets in the cortex and hippocampus of CSD‐treated mice. Moreover, GE treatment significantly suppressed CSD‐induced NF‐κB p65, iNOS, and COX‐2 activation in the cortex and hippocampus, as well as inhibited CSD‐induced pro‐inflammatory cytokines (TNF‐α, IL‐6, and IL‐1β) release in the serum. Taken together, all these results suggested that GE has substantial potential as a therapeutic intervention for the alleviation of CSD‐induced deleterious effects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective effects of Genistein on the cognitive deficits induced by chronic sleep deprivation

Lü

Jiang

et al. 2020

Phytotherapy Research

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“…Melatonin, a pineal hormone that controls circadian rhythm, also relies upon autophagy pathways and mTOR to control processes of aging and neurodegeneration (3). Loss of mTOR activation may be involved with altered circadian rhythm and cognitive decline during prolonged space flight (96). Cerebral ischemic infarction also may be influenced by alteration in circadian rhythm genes and fluctuations in mTOR activity (66, 97).…”

Section: Circadian Rhythm Mtor and Sirt1mentioning

confidence: 99%

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

Maiese¹

2017

CNR

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Background The mammalian circadian clock and its associated clock genes are increasingly be recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease. Methods In light of the significant role circadian rhythm can hold over the body's normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis. Results In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer's disease and Parkinson's disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth. Conclusions Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.

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“…mTOR also is known as the mammalian target of rapamycin and the FK506-binding protein 12-rapamycin complex-associated protein 1. mTOR controls multiple functions that determine the transcription of genes, proliferation and senescence of cells, protein formation, cellular metabolism, and cellular longevity (9, 57, 77, 129, 130). Melatonin, a pineal hormone that controls circadian rhythm, relies upon autophagy pathways and mTOR to control processes of aging and neurodegeneration (131).…”

Section: Circadian Clock Genesmentioning

confidence: 99%

“…Melatonin, a pineal hormone that controls circadian rhythm, relies upon autophagy pathways and mTOR to control processes of aging and neurodegeneration (131). Loss of mTOR activation can be involved with altered circadian rhythm and cognitive decline during prolonged space flight (130). Furthermore, cerebral ischemic infarction may be influenced by an alteration in circadian rhythm genes and fluctuations in mTOR activity (126, 132).…”

Section: Circadian Clock Genesmentioning

confidence: 99%

Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors

Maiese¹

2018

CNR

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BACKGROUND With the global increase in life span expectancy, neurodegenerative disorders continue to affect an ever increasing number of individuals throughout the world. New treatment strategies for neurodegenerative diseases are desperately required given the lack of current treatment modalities. METHODS Here we examine novel strategies for neurodegenerative disorders that include circadian clock genes, non-coding ribonucleic acids (RNAs), and the mammalian forkhead transcription factors of the O class (FoxOs). RESULTS Circadian clock genes, non-coding RNAs, and FoxOs offer exciting prospects to potentially limit or remove the significant disability and death associated with neurodegenerative disorders. Each of these pathways have an intimate relationship with the programmed death pathways of autophagy and apoptosis and share a common link to the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) and the mechanistic target of rapamycin (mTOR). Circadian clock genes are necessary to modulate autophagy, limit cognitive loss, and prevent neuronal injury. Non-coding RNAs can control neuronal stem cell development and neuronal differentiation and offer protection against vascular disease such as atherosclerosis. FoxOs provide exciting prospects to block neuronal apoptotic death and to activate pathways of autophagy to remove toxic accumulations in neurons that can lead to neurodegenerative disorders. CONCLUSIONS Continued work with circadian clock genes, non-coding RNAs, and FoxOs can offer new prospects and hope for the development of vital strategies for the treatment of neurodegenerative diseases. These innovative investigative avenues have the potential to significantly limit disability and death from these devastating disorders.

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Dammarane Sapogenins Ameliorates Neurocognitive Functional Impairment Induced by Simulated Long-Duration Spaceflight

Cited by 45 publications

References 75 publications

Protective effects of Genistein on the cognitive deficits induced by chronic sleep deprivation

Protective effects of Genistein on the cognitive deficits induced by chronic sleep deprivation

Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer

Novel Treatment Strategies for the Nervous System: Circadian Clock Genes, Non-coding RNAs, and Forkhead Transcription Factors

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