Antioxidant therapy reverses sympathetic dysfunction, oxidative stress, and hypertension in male hyperadipose rats

Lopes, Fernanda Novi Cortegoso; Bellinati, Natália Veronez da Cunha; Campos, Blenda Hyedra de; Fattori, Victor; Cecchini, Rúbens; Verri, Waldiceu Aparecido; Pinge‐Filho, Phileno; Martins‐Pinge, Marli Cardoso

doi:10.1016/j.lfs.2022.120405

Cited by 16 publications

(5 citation statements)

References 57 publications

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“…In obese conditions, the vagus and parasympathetic nerves may be damaged due to ferroptosis, which also promotes further sympathetic activity and autonomic nervous system imbalance. Furthermore, studies have found that antioxidants can reverse sympathetic dysfunction, oxidative stress, and hypertension in male obese rats following intervention with antioxidants ( 122 ). It has also been shown that impaired baroreceptor reflexes are caused by reduced inhibition of the vagus and parasympathetic nerves ( 123 ).…”

Section: Sympathetic Nervementioning

confidence: 99%

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

et al. 2022

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Ferroptosis requires not only the accumulation of iron ions, but also changes in many ferroptosis-related regulators, including a decrease in GPX4 and inhibition of SLC7A11 for classical ferroptosis, a deletion of FSP1 or GCH1. Surprisingly, adipose tissue (AT) in the obesity conditions is also accompanied by iron buildup, decreased GSH, and increased ROS. On the neurological side, the pro-inflammatory factor released by AT may have first caused ferroptosis in the vagus nerve by inhibiting of the NRF2-GPX4 pathway, resulting in disorders of the autonomic nervous system. On the immune side, obesity may cause M2 macrophages ferroptosis due to damage to iron-rich ATMs (MFehi) and antioxidant ATMs (Mox), and lead to Treg cells ferroptosis through reductions in NRF2, GPX4, and GCH1 levels. At the same time, the reduction in GPX4 may also trigger the ferroptosis of B1 cells. In addition, some studies have also found the role of GPX4 in neutrophil autophagy, which is also worth pondering whether there is a connection with ferroptosis. In conclusion, this review summarizes the associations between neuroimmune regulation associated with obesity and ferroptosis, and on the basis of this, highlights their potential molecular mechanisms, proposing that ferroptosis in one or more cells in a multicellular tissue changes the fate of that tissue.

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Section: Sympathetic Nervementioning

confidence: 99%

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

et al. 2022

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“…Neurogenic hypertension, regulated by the central nervous system, particularly the rostral ventrolateral medulla (RVLM), [1] has the characteristics of chronic sympathetic outflow and persistent elevation in blood pressure (BP), [2] resulting in stroke, [3] kidney failure, [4] and cardiovascular diseases, including myocardial fibrosis, infarction, coronary heart diseases, and heart failure. [5] The pathogenic mechanism of neurogenic hypertension is multifactor, and one of the important contributing factors is reactive oxygen species (ROS), involving superoxide radicals ( * O 2 À ), hydrogen peroxides (H 2 O 2 ), and hydroxyl radical ( * OH), which contributes to mitochondria stress, inflammation, and deoxyribonucleic acid (DNA) degradation.…”

Section: Introductionmentioning

confidence: 99%

Ultrathin Niobium Carbide MXenzyme for Remedying Hypertension by Antioxidative and Neuroprotective Actions

Yang

Xia

et al. 2023

Angew Chem Int Ed

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Hypertension, as a leading risk factor for cardiovascular diseases, is associated with oxidative stress and impairment of endogenous antioxidant mechanisms, but there is still a tremendous knowledge gap between hypertension treatment and nanomedicines. Herein, we report a specific nanozyme based on ultrathin two‐dimensional (2D) niobium carbide (Nb2C) MXene, termed Nb2C MXenzyme, to fight against hypertension by achieving highly efficient reactive oxygen species elimination and inflammatory factors inhibition. The biocompatible Nb2C MXenzyme displays multiple enzyme‐mimicking activities, involving superoxide dismutase, catalase, glutathione peroxidase, and peroxidase, inducing cytoprotective effects by resisting oxidative stress, thereby alleviating inflammatory response and reducing blood pressure, which is systematically demonstrated in a stress‐induced hypertension rat model. This strategy not only opens new opportunities for nanozymes to treat hypertension but also expands the potential biomedical applications of 2D MXene nanosystems.

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“…With such an enormous appetite for this additive in the food industry, the health concerns are also substantial given that MSG administration increases the number of pachytene stage cells in primary spermatocytes [ 12 , 13 ] and induces OS [ 14 , 15 ] and free radical generation [ 16 , 17 ]. In addition, obesity [ 18 , 19 , 20 , 21 ], disorders of the central nervous system [ 10 , 22 , 23 ], hepatic damage [ 24 , 25 , 26 ], reproductive malfunctions [ 12 , 27 , 28 , 29 ], cardiovascular diseases [ 30 , 31 ], and hypertension [ 32 , 33 , 34 ] are considered to be some of the major side effects of MSG.…”

Section: Introductionmentioning

confidence: 99%

Monosodium Glutamate Perturbs Human Trophoblast Invasion and Differentiation through a Reactive Oxygen Species-Mediated Pathway: An In-Vitro Assessment

et al. 2023

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The overproduction of reactive oxygen species (ROS) has been associated with various human diseases. ROS exert a multitude of biological effects with both physiological and pathological consequences. Monosodium glutamate (MSG), a sodium salt of the natural amino acid glutamate, is a flavor-enhancing food additive, which is widely used in Asian cuisine and is an ingredient that brings out the “umami” meat flavor. MSG consumption in rats is associated with ROS generation. Owing to its consumption as part of the fast-food culture and concerns about its possible effects on pregnancy, we aimed to study the impact of MSG on placental trophoblast cells. MSG exposure influenced trophoblast invasion and differentiation, two of the most critical functions during placentation through enhanced production of ROS. Similar findings were also observed on MSG-treated placental explants, as confirmed by elevated Nrf2 levels. Ultrastructural studies revealed signs of subcellular injury by MSG exposure. Mechanistically, MSG-induced oxidative stress with endoplasmic reticulum stress pathways involving Xbp1s and IRE1α was observed. The effect of MSG through an increased ROS production indicates that its long-term exposure might have adverse health effect by compromising key trophoblast functions.

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Antioxidant therapy reverses sympathetic dysfunction, oxidative stress, and hypertension in male hyperadipose rats

Cited by 16 publications

References 57 publications

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

Ultrathin Niobium Carbide MXenzyme for Remedying Hypertension by Antioxidative and Neuroprotective Actions

Monosodium Glutamate Perturbs Human Trophoblast Invasion and Differentiation through a Reactive Oxygen Species-Mediated Pathway: An In-Vitro Assessment

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