Taurine inhibits neuron apoptosis in hippocampus of diabetic rats and high glucose exposed HT-22 cells via the NGF-Akt/Bad pathway

Wu, Pingan; Shi, Xiaoxia; Luo, Ming; Inamullah, .; Li, Kaixin; Zhang, Mengren; Ma, Jingran; Li, Yuan; Liu, Yanqing; Zhang, Cong; Liu, Xiaofang; Li, Shuangyue; Li, Qiujuan; Chen, Xiaochi; Che, Xiangyu; Piao, Fengyuan

doi:10.1007/s00726-019-02810-6

Cited by 23 publications

(14 citation statements)

References 52 publications

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“…We further revealed that L -BAIBA ameliorates H 2 O 2 -induced apoptosis in PC12 cells via activation of the AMPK and PI3K /Akt pathways. Although Akt did not significantly affect the inhibitory effects of L -BAIBA on H 2 O 2 -induced ROS production, Akt is a key mediator of cell survival( Manning and Cantley, 2007 ); it is a crucial factor that attenuates neuronal apoptosis ( Chen et al, 2020 , Okada et al, 2019 , Wu et al, 2020 ). Akt promotes cell survival by blocking the function of pro-apoptotic proteins and processes.…”

Section: Discussionmentioning

confidence: 98%

β-Aminoisobutyric acid, L-BAIBA, protects PC12 cells from hydrogen peroxide-induced oxidative stress and apoptosis via activation of the AMPK and PI3K/Akt pathway

Minato

Nakamura

Saiki

et al. 2022

IBRO Neuroscience Reports

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β-Aminoisobutyric acid (BAIBA) is a myokine that is secreted from skeletal muscles by the exercise. Recently, increasing evidence has suggested the multifocal physiological activities of BAIBA. In this study, we investigated whether L -BAIBA has protective effects on rat pheochromocytoma (PC12) cells. Cultured PC12 cells were stimulated with L -BAIBA. Western blot analyses revealed that L -BAIBA stimulation significantly increased the phosphorylation of AMPK and Akt. In contrast, no effect was observed on neurite outgrowth by L -BAIBA. To investigate the effects of L -BAIBA on oxidative stress, PC 12 cells were exposed to hydrogen peroxide (H 2 O 2 ) with and without L-BAIBA. Hydrogen peroxide significantly increased reactive oxygen species (ROS) production and apoptosis in PC12 cells. Pretreatment with L -BAIBA suppressed H 2 O 2 -induced ROS production and apoptosis, which was abolished by the inhibition of AMPK by compound C. On the other hand, the inhibitory effects of L -BAIBA on oxidative stress-induced apoptosis were abolished by the inhibition of both AMPK and PI3K/Akt. In conclusion, we demonstrated that L -BAIBA confers protection against oxidative stress in PC12 cells by activating the AMPK and PI3K/Akt pathways. These results suggest that L -BAIBA may play a crucial role on protection of neuron-like cells and become a pharmacological agent to treat neuronal diseases.

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Section: Discussionmentioning

confidence: 98%

β-Aminoisobutyric acid, L-BAIBA, protects PC12 cells from hydrogen peroxide-induced oxidative stress and apoptosis via activation of the AMPK and PI3K/Akt pathway

Minato

Nakamura

Saiki

et al. 2022

IBRO Neuroscience Reports

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“…Recently, Wu et al experimentally induced NGF overexpression in a hippocampal neuronal cell line by taurine administration, observing an increase in TrkA and Akt phosphorylation and, consequently, a significant reduction in apoptosis. The same NGF expression changes were also observed after taurine administration in rats, in association with an improvement in learning and memory, suggesting taurine as a potential candidate against cognitive impairment through inhibition of hippocampal neuronal apoptosis [ 57 ].…”

Section: Effects Of Physical Exercise On Brain Healthmentioning

confidence: 83%

Physical Exercise and Health: A Focus on Its Protective Role in Neurodegenerative Diseases

Bonanni

Cariati

Tarantino

et al. 2022

JFMK

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Scientific evidence has demonstrated the power of physical exercise in the prevention and treatment of numerous chronic and/or age-related diseases, such as musculoskeletal, metabolic, and cardiovascular disorders. In addition, regular exercise is known to play a key role in the context of neurodegenerative diseases, as it helps to reduce the risk of their onset and counteracts their progression. However, the underlying molecular mechanisms have not yet been fully elucidated. In this regard, neurotrophins, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glia cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4), have been suggested as key mediators of brain health benefits, as they are involved in neurogenesis, neuronal survival, and synaptic plasticity. The production of these neurotrophic factors, known to be increased by physical exercise, is downregulated in neurodegenerative disorders, suggesting their fundamental importance in maintaining brain health. However, the mechanism by which physical exercise promotes the production of neurotrophins remains to be understood, posing limits on their use for the development of potential therapeutic strategies for the treatment of neurodegenerative diseases. In this literature review, we analyzed the most recent evidence regarding the relationship between physical exercise, neurotrophins, and brain health, providing an overview of their involvement in the onset and progression of neurodegeneration.

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“…In a type II diabetes mellitus rat model, intracellular taurine has proven to inhibit neuronal apoptosis in the brain, more specifically in the hippocampal CA1 pyramidal cells by acting on the NGF/Akt/Bad pathway ( Wu et al, 2020 ). The addition of taurine to rat’s hippocampal cultured neurons increased the expression of nerve growth factor (NGF) and augmented phosphorylation of the NGF receptor, tyrosine kinase receptor type A (TrkA), activating an important anti-apoptotic pathway.…”

Section: Neuroprotective Effects Of Taurine Released From Astrocytesmentioning

confidence: 99%

Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship

Ramírez-Guerrero

Guardo-Maya

Medina-Rincón

et al. 2022

Front. Mol. Neurosci.

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Taurine is considered the most abundant free amino acid in the brain. Even though there are endogenous mechanisms for taurine production in neural cells, an exogenous supply of taurine is required to meet physiological needs. Taurine is required for optimal postnatal brain development; however, its brain concentration decreases with age. Synthesis of taurine in the central nervous system (CNS) occurs predominantly in astrocytes. A metabolic coupling between astrocytes and neurons has been reported, in which astrocytes provide neurons with hypotaurine as a substrate for taurine production. Taurine has antioxidative, osmoregulatory, and anti-inflammatory functions, among other cytoprotective properties. Astrocytes release taurine as a gliotransmitter, promoting both extracellular and intracellular effects in neurons. The extracellular effects include binding to neuronal GABAA and glycine receptors, with subsequent cellular hyperpolarization, and attenuation of N-methyl-D-aspartic acid (NMDA)-mediated glutamate excitotoxicity. Taurine intracellular effects are directed toward calcium homeostatic pathway, reducing calcium overload and thus preventing excitotoxicity, mitochondrial stress, and apoptosis. However, several physiological aspects of taurine remain unclear, such as the existence or not of a specific taurine receptor. Therefore, further research is needed not only in astrocytes and neurons, but also in other glial cells in order to fully comprehend taurine metabolism and function in the brain. Nonetheless, astrocyte’s role in taurine-induced neuroprotective functions should be considered as a promising therapeutic target of several neuroinflammatory, neurodegenerative and psychiatric diseases in the near future. This review provides an overview of the significant relationship between taurine and astrocytes, as well as its homeostatic and neuroprotective role in the nervous system.

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Taurine inhibits neuron apoptosis in hippocampus of diabetic rats and high glucose exposed HT-22 cells via the NGF-Akt/Bad pathway

Cited by 23 publications

References 52 publications

β-Aminoisobutyric acid, L-BAIBA, protects PC12 cells from hydrogen peroxide-induced oxidative stress and apoptosis via activation of the AMPK and PI3K/Akt pathway

β-Aminoisobutyric acid, L-BAIBA, protects PC12 cells from hydrogen peroxide-induced oxidative stress and apoptosis via activation of the AMPK and PI3K/Akt pathway

Physical Exercise and Health: A Focus on Its Protective Role in Neurodegenerative Diseases

Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship

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