Betaine reverses the memory impairments in a chronic cerebral hypoperfusion rat model

Nie, Chunjie; Nie, Heng–Yong; Zhao, Yin; Wu, Jianzhao; Zhang, Xiaojian

doi:10.1016/j.neulet.2015.11.019

Cited by 32 publications

(19 citation statements)

References 34 publications

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“…Previous studies demonstrated that cerebral hypoperfusion could lead to oxidative stress, neuroinflammation, neurotransmitter system dysfunction, mitochondrial dysfunction, disturbance of lipid metabolism, and alterations of growth factor (Du et al, 2017). Oxidative stress plays an important role in cognitive deficits induced by the chronic cerebral hypoperfusion (Chunjiea et al, 2016). Neuroinflammation characterized by Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)α plays an important role in VD (Belkhelfa et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Transcranial Direct Current Stimulation Ameliorates Cognitive Impairment via Modulating Oxidative Stress, Inflammation, and Autophagy in a Rat Model of Vascular Dementia

et al. 2020

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To investigate the potential applications and the molecular mechanisms of transcranial direct current stimulation (tDCS) on cognitive impairment in a vascular dementia (VD) animal model. Sprague-Dawley rats were used in this study. VD rat model was induced by modified permanent bilateral common carotid artery occlusion (2-VO) approach. Anodal tDCS was applied to the animals. Morris water maze was used to analyze spatial memory and navigation ability. The pathological changes in the hippocampal CA1 region and cerebral cortex were examined via Hematoxylin-Eosin staining. The rats were sacrificed for the measurement of the level of superoxide (SOD), glutathione (GSH), reactive oxidative species (ROS), malondialdehyd (MDA), Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α level in the hippocampus. Western blot was carried out to measure the hippocampal expression of microtubule-associated protein 1 light chain 3 (LC-3) and p62. Rats with VD have decreased number of neurons in the hippocampus and cerebral cortex, as well as worse cognitive impairment. The proliferation of activated microglia and astroglia, accompanied with attenuation of myelination were observed in the white matter about 1 month after 2-VO operation. These abnormalities were significantly ameliorated by tDCS treatment. Further study revealed that anodal tDCS could suppress the MDA and ROS level, while enhance the SOD and GSH level to reduce the oxidative stress. Anodal tDCS could inhibit hypoperfusion-induced IL-1β, IL-6, and TNF-α expression to attenuate inflammatory response in hippocampus. Moreover, anodal tDCS treatment could alleviate autophagy level. The study has demonstrated a possible therapeutic role of tDCS in the treatment of cognitive impairment in VD.

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Section: Introductionmentioning

confidence: 99%

Transcranial Direct Current Stimulation Ameliorates Cognitive Impairment via Modulating Oxidative Stress, Inflammation, and Autophagy in a Rat Model of Vascular Dementia

et al. 2020

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“…Some authors reported treatment with betaine in rats significantly decreased the MDA level (Sehirli et al 2016). Betaine could reduce the oxidative stress by suppressing MDA and enhancing SOD in rat brain (Nie et al 2016). Superoxide dismutase (SOD) and catalase (CAT) constitute the primary enzymatic antioxidant defense against ROS-induced oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Betaine protects against heat exposure–induced oxidative stress and apoptosis in bovine mammary epithelial cells via regulation of ROS production

Wang

et al. 2019

Cell Stress and Chaperones

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Heat stress is one of the wide varieties of factors which cause oxidative stress in vivo; elevated temperature can lead to oxidative stress of dairy cows that affects milk production. The aim of this study was to determine the capacity of the betaine to act as an antioxidant against oxidative stress induced by heat exposure and apoptosis in mammary epithelial cells (mammary alveolar cells, MAC-T). The MAC-T were divided into four treatment groups: control (37 °C), heat stress (HS, 42 °C), betaine (37 °C), and HS + betaine. MAC-T under heat stress (HS) showed increased ROS accumulation, malondialdehyde (MDA) content, superoxide dismutase (SOD) concentration, and catalase (CAT) activity. During heat stress, betaine decreased the mRNA expression level of HSP70 and HSP27 in MAC-T. Bax/Bcl-2 ratio and caspase-3, the markers of apoptosis, were also elevated in MAC-T under heat stress. The markers of oxidative stress Nrf-2/HO-1 genes were also elevated in MAC-T under heat stress. Pretreatment of betaine reversed the heat-induced depletion in total antioxidant status, ROS accumulation, and SOD and CAT contents in MAC-T. Bax/Bcl-2 ratio and Nrf-2/HO-1 expression of heat-exposed MAC-T were also reduced with betaine supplementation. In conclusion, betaine alleviated oxidative stress and apoptosis of MAC-T by inhibiting ROS accumulation.

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“…In this study, we observed reduced glutathione levels and elevated betaine levels, both of which are differential metabolites in cells. Glutathione is a major redox "buffer" in the cytoplasm [43], while betaine is widely considered as an antioxidant that can alleviate oxidative stress [44] [45]. Therefore, we predicted that after treatment with retinol at the IC 50 , the large amount of RET entering the cells could cause mitochondrial dysfunction and lipid peroxidation to result in massive superoxide anion production because of the leakage of the electron transport chain, thereby leading to oxidative stress responses.…”

Section: Discussionmentioning

confidence: 99%

Effect of IC50 dose of retinol on metabolomics of RAW264.7 cells

Wang

Song

Geng

2019

Preprint

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Background: Vitamin A is one of the most multifunctional Vitamin in the human body and is involved in several basic physiological processes from embryonic development to adulthood, such as embryogenesis, vision, immunity, cell differentiation, and proliferation. The aim of current study was to identify its effects on the differential metabolites and main metabolic pathways. We also analyzed the toxicity of retinol.Methods: In this study, we conducted proton nuclear magnetic resonance (NMR) to evaluate metabolomic changes in RAW264.7 cells after treatment with retinol at a half maximal inhibitory concentration (IC 50 ).Results: Our results showed that the IC 50 dose (140 μM) of retinol affected the metabolism of RAW264.7 cells, with a total of 22 differential metabolites identified via 1 H-NMR, including amino acids, sugars, organic acids, glutathione, glycerin, and creatine. Additionally, multiple metabolic pathways were affected by retinol treatment, including amino acid biosynthesis, protein synthesis, and pyruvate metabolism. We speculate that the cytotoxicity of retinol at the IC 50 dose is attributed to mitochondrial dysfunction as a result of oxidative stress or lipid peroxidation.Conclusions: RAW264.7 cells showed significant changes in protein biosynthesis, urea cycle, arginine and proline metabolism, malate-aspartate shuttle, alanine metabolism, and cellular respiration after treatment with retinol at the IC 50 dose (140 μM), indicating that retinol affects cellular physiological functions via different metabolic pathways.

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Betaine reverses the memory impairments in a chronic cerebral hypoperfusion rat model

Cited by 32 publications

References 34 publications

Transcranial Direct Current Stimulation Ameliorates Cognitive Impairment via Modulating Oxidative Stress, Inflammation, and Autophagy in a Rat Model of Vascular Dementia

Transcranial Direct Current Stimulation Ameliorates Cognitive Impairment via Modulating Oxidative Stress, Inflammation, and Autophagy in a Rat Model of Vascular Dementia

Betaine protects against heat exposure–induced oxidative stress and apoptosis in bovine mammary epithelial cells via regulation of ROS production

Effect of IC50 dose of retinol on metabolomics of RAW264.7 cells

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