Protective effect of gamma‐aminobutyric acid against oxidative stress by inducing phase II enzymes in C2C12 myoblast cells

Choe, Hyeonjeong; Lee, Hana; Lee, Junsoo; Kim, Young-Hwa

doi:10.1111/jfbc.13639

Cited by 12 publications

(6 citation statements)

References 49 publications

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“…These results indicate that both the cAMP-PKA signaling pathway and GABA-GABA A receptor signaling mediate the effects of DEX in inhibiting NADPH-derived superoxide production and sympathetic activation in LPS-induced sepsis. The findings were supported by previous findings that cAMP-PKA signaling contributes to ROS production [ 57 , 58 ], and that GABA attenuates oxidative stress [ 59 , 60 , 61 ].…”

Section: Discussionsupporting

confidence: 86%

Dexmedetomidine Attenuates Lipopolysaccharide-Induced Sympathetic Activation and Sepsis via Suppressing Superoxide Signaling in Paraventricular Nucleus

Wang

et al. 2022

Antioxidants

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Sympathetic overactivity contributes to the pathogenesis of sepsis. The selective α2-adrenergic receptor agonist dexmedetomidine (DEX) is widely used for perioperative sedation and analgesia. We aimed to determine the central roles and mechanisms of DEX in attenuating sympathetic activity and inflammation in sepsis. Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS) in rats. Effects of DEX were investigated 24 h after injection of LPS. Bilateral microinjection of DEX in the paraventricular nucleus (PVN) attenuated LPS-induced sympathetic overactivity, which was attenuated by the superoxide dismutase inhibitor DETC, cAMP analog db-cAMP or GABAA receptor antagonist gabazine. Superoxide scavenger tempol, NADPH oxidase inhibitor apocynin, adenylate cyclase inhibitor SQ22536 or PKA inhibitor Rp-cAMP caused similar effects to DEX in attenuating LPS-induced sympathetic activation. DEX inhibited LPS-induced superoxide and cAMP production, as well as NADPH oxidase, adenylate cyclase and PKA activation. The roles of DEX in reducing superoxide production and NADPH oxidase activation were attenuated by db-cAMP or gabazine. Intravenous infusion of DEX inhibited LPS-induced sympathetic overactivity, NOX activation, superoxide production, TNF-α and IL-1β upregulation in the PVN and plasma, as well as lung and renal injury, which were attenuated by the PVN microinjection of yohimbine and DETC. We conclude that activation of α2-adrenergic receptors with DEX in the PVN attenuated LPS-induced sympathetic overactivity by reducing NADPH oxidase-dependent superoxide production via both inhibiting adenylate cyclase-cAMP-PKA signaling and activating GABAA receptors. The inhibition of NADPH oxidase-dependent superoxide production in the PVN partially contributes to the roles of intravenous infusion of DEX in attenuating LPS-induced sympathetic activation, oxidative stress and inflammation.

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Section: Discussionsupporting

confidence: 86%

Dexmedetomidine Attenuates Lipopolysaccharide-Induced Sympathetic Activation and Sepsis via Suppressing Superoxide Signaling in Paraventricular Nucleus

Wang

et al. 2022

Antioxidants

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“…GABA also plays a role in protecting cells against reactive oxygen species (ROS) by regulating the activity of various antioxidants. Thus, the reduced GABAergic activity in patients with BD described by some researchers could contribute to the damage in the CNS regions associated with the BD symptoms by reducing the antioxidant capacity [ 222 , 223 ].…”

Section: Resultsmentioning

confidence: 99%

Is SARS-CoV-2 a Risk Factor of Bipolar Disorder?—A Narrative Review

Lorkiewicz

Waszkiewicz

2022

JCM

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For 2.5 years we have been facing the coronavirus disease (COVID-19) and its health, social and economic effects. One of its known consequences is the development of neuropsychiatric diseases such as anxiety and depression. However, reports of manic episodes related to COVID-19 have emerged. Mania is an integral part of the debilitating illness—bipolar disorder (BD). Due to its devastating effects, it is therefore important to establish whether SARS-CoV-2 infection is a causative agent of this severe mental disorder. In this narrative review, we discuss the similarities between the disorders caused by SARS-CoV-2 and those found in patients with BD, and we also try to answer the question of whether SARS-CoV-2 infection may be a risk factor for the development of this affective disorder. Our observation shows that disorders in COVID-19 showing the greatest similarity to those in BD are cytokine disorders, tryptophan metabolism, sleep disorders and structural changes in the central nervous system (CNS). These changes, especially intensified in severe infections, may be a trigger for the development of BD in particularly vulnerable people, e.g., with family history, or cause an acute episode in patients with a pre-existing BD.

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“…A clinical study showed that the level of GABA in the brain of PD patients was significantly lower than that of healthy controls ( Song et al., 2021 ), which resulted in the dopaminergic pathology of PD. GABA treatment increased the expression level of Nrf2 and the activity of antioxidant enzymes, such as CAT and SOD, effectively reducing the consumption of glutathione and the level of ROS and thereby reducing oxidative stress ( Zhu et al., 2019 ; Choe et al., 2021 ). Excessive GABA in astrocytes caused the loss of TH, which showed a decrease in the discharge of dopaminergic neurons, while blocking the astrocytic GABA synthesis could reverse this effect ( Heo et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…Mounting evidence showed that the concentration of GABA was decreased in many neuropsychiatric diseases ( Zheng et al., 2017 ; Cortès-Saladelafont et al., 2018 ), and there was a negative correlation between the GABA level in the cerebral cortex and the severity of PD symptoms ( van Nuland et al., 2020 ). It was reported that GABA treatment can increase the expression of Nrf2 protein in the nucleus of myoblasts and regulate the level of glutathione and glycogen synthase kinase-3β phosphorylates as well as the activity of catalase (CAT), superoxide dismutase (SOD), and ROS scavenging ( Choe et al., 2021 ) and prevent the H 2 O 2 -induced transfer of Nrf2 into the nucleus, thus further alleviating oxidative stress injury and restoring the redox homeostasis of cells ( Tang et al., 2018 ). Moreover, GABA can reverse the H 2 O 2 -induced mRNA expression and protein expression of Keap1 and Nrf2 and protect endothelial cells from oxidative stress damage by regulating the Nrf2 signaling pathway ( Zhu et al., 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Probiotic Pediococcus pentosaceus ameliorates MPTP-induced oxidative stress via regulating the gut microbiota–gut–brain axis

Pan

Wei

Yuan

et al. 2022

Front. Cell. Infect. Microbiol.

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Recent evidence demonstrated that functional bacteria were involved in the regulation of Parkinson’s disease (PD). However, the mechanism of probiotics in improving PD was unclear. Here the antioxidant effect and the mechanism of probiotics Pediococcus pentosaceus (PP) on PD were studied by regulating the gut–brain axis. In this study, male C57BL/6J mice were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intraperitoneally to establish a PD model and were then treated with PP for 4 weeks. Subsequently, a series of neurobehavioral tests to evaluate the motor function of the mice was performed. Additionally, degeneration of dopaminergic neurons, accumulation of α-synuclein, the production of an oxidative stress response, and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway-related proteins were evaluated. Moreover, the gut microbial composition and the level of metabolite γ-aminobutyric acid (GABA) were assessed. The results showed that PP treatment could improve MPTP-induced motor deficits, the degeneration of dopaminergic neurons, and the accumulation of α-synuclein. Moreover, PP treatment significantly increased the levels of SOD1, Gpx1, and Nrf2, while it decreased the levels of Keap1 in the brain of MPTP-induced mice. Notably, PP treatment improved the gut microbial dysbiosis and increased the level of GABA in MPTP-induced mice. These findings indicated that PP might represent a promising candidate, due to the metabolite of GABA, that could be used for the treatment of PD.

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Protective effect of gamma‐aminobutyric acid against oxidative stress by inducing phase II enzymes in C2C12 myoblast cells

Cited by 12 publications

References 49 publications

Dexmedetomidine Attenuates Lipopolysaccharide-Induced Sympathetic Activation and Sepsis via Suppressing Superoxide Signaling in Paraventricular Nucleus

Dexmedetomidine Attenuates Lipopolysaccharide-Induced Sympathetic Activation and Sepsis via Suppressing Superoxide Signaling in Paraventricular Nucleus

Is SARS-CoV-2 a Risk Factor of Bipolar Disorder?—A Narrative Review

Probiotic Pediococcus pentosaceus ameliorates MPTP-induced oxidative stress via regulating the gut microbiota–gut–brain axis

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