Hydrogen sulfide prevents the vascular dysfunction induced by severe traumatic brain injury in rats by reducing reactive oxygen species and modulating eNOS and H2S-synthesizing enzyme expression

López-Preza, Félix I.; Cruz, Saúl Huerta de la; Santiago-Castañeda, Cindy; Silva‐Velasco, Diana L.; Beltrán-Ornelas, Jesús H.; Tapia-Martínez, Jorge; Sánchez-López, Araceli; Rocha, Luisa; Centurión, David

doi:10.1016/j.lfs.2022.121218

Cited by 13 publications

(11 citation statements)

References 81 publications

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“…In this sense, our study shows alteration of oxidative stress and differential relaxant responses to CCh and SNP; it is necessary to mention that our findings are in concordance with previous studies. 43,68,69 Taken together, our results and previous studies suggest that increasing oxidative stress affects mainly the endothelium instead of the smooth muscle, affecting production and not the NO pathway signaling. However, H 2 S is a scavenger of ROS because of its reductive potential acting as an antioxidant.…”

Section: Discussionsupporting

confidence: 82%

“…In this relation, the activity of superoxide dismutase has been shown to be negatively correlated with noradrenaline-induced maximal contractions in rats with chronic stress. 59 Importantly, the treatment with NaHS restored the contractile responses to NE in the thoracic aorta, as observed in other studies involving traumatic brain injury 43 and diabetes. 26,42 Moreover, CRS attenuated the CCh-induced vasorelaxation in thoracic aortas, indicating an impairment in NO synthesis or signaling pathway.…”

Section: Nahs Administration Reestablishes Hemodynamic Variables and ...supporting

confidence: 72%

“…Although it has been shown that GYY 4137, an organic H 2 S donor, promotes food intake under physiological conditions, 41 previous studies have indicated that H 2 S donors do not reverse the body weight loss observed in diabetes 42 or traumatic brain injury. 43 Thus, it appears that H 2 S may not play a role in regulating body weight under pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

“…9 Moreover, the reestablishment of endothelial-dependent relaxation is a mechanism underlying the antihypertensive effect of NaHS. 43 Therefore, we further investigated the effects of NaHS treatment on the vascular dysfunction induced by chronic stress. We found that CRS increased the vasocontractile responses induced by NE in the thoracic aorta, as previously shown for other blood vessels.…”

Section: Discussionmentioning

confidence: 99%

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Sodium Hydrosulfide Reverts Chronic Stress–Induced Cardiovascular Alterations by Reducing Oxidative Stress

Beltran-Ornelas,

Silva-Velasco,

Tapia-Martínez

et al. 2024

Journal of Cardiovascular Pharmacology

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Chronic stress induces a group of unrecognized cardiovascular impairments, including elevated hemodynamic variables and vascular dysfunction. Moreover, hydrogen sulfide (H2S), a gasotransmitter that regulates the cardiovascular system, decreases under chronic stress. Thus, this study assessed the impact of NaHS (H2S donor) on chronic restraint stress (CRS)-induced cardiovascular changes. For that purpose, male Wistar rats were restrained for 2 h in a transparent acrylic tube over eight weeks. Then, body weight, relative adrenal gland weight, serum corticosterone, H2S-synthesizing enzymes, eNOS expression, reactive oxygen species (ROS) levels, lipid peroxidation, and reduced glutathione/oxidized glutathione (GSH2/GSSG) ratio, were determined in the thoracic aorta. The hemodynamic variables were measured in vivo by the plethysmograph method. The vascular function was evaluated in vitro as vasorelaxant responses induced by carbachol (CCh) or sodium nitroprusside, and norepinephrine (NE)-mediated vasocontractile responses in the thoracic aorta. CRS increased: (1) relative adrenal gland weight; (2) hemodynamic variables; (3) vasoconstrictor responses induced by NE, (4) ROS levels, and (5) lipid peroxidation in the thoracic aorta. Additionally, CRS decreased: (1) body weight; (2) vasorelaxant responses induced by CCh; (3) GSH content and (4) GSH2/GSSG ratio. Notably, NaHS administration (5.6 mg/kg) restored hemodynamic variables, lipid peroxidation and attenuated the vasoconstrictor responses induced by NE in the thoracic aorta. In addition, NaHS treatment increased relative adrenal gland weight and the GSH2/GSSG ratio. Taken together, our results demonstrate that NaHS alleviates CRS-induced hypertension by reducing oxidative stress and restoring vascular function in the thoracic aorta.

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Section: Discussionsupporting

confidence: 82%

Section: Nahs Administration Reestablishes Hemodynamic Variables and ...supporting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Sodium Hydrosulfide Reverts Chronic Stress–Induced Cardiovascular Alterations by Reducing Oxidative Stress

Beltran-Ornelas,

Silva-Velasco,

Tapia-Martínez

et al. 2024

Journal of Cardiovascular Pharmacology

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“…The level of H 2 S in the brain has been shown to decrease in the early stage (12-24 h) and recover in the late stage during 3 to 7 days following TBI (21,22). Exogenous administration of H 2 S prevents vascular dysfunction and the development of hemodynamic impairments after TBI (23,24). These evidences suggested that H 2 S administration had a protective effect against TBI.…”

Section: Introductionmentioning

confidence: 97%

Dynamic Changes and Effects of H2S, IGF-1, and GH in The Traumatic Brain Injury

Zhang

Kong

et al. 2023

Preprint

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Background: The goal of this investigation was to examine the expression changes of H2S, IGF-1, and GH after TBI and to detect their roles after TBI. Methods: In this study, we first collected cerebrospinal fluid (CSF) and plasma from TBI patients at different times after injury and evaluated the concentrations of H2S, IGF-1, and GH. In vitro TBI conditions were stimulated by using HT22 hippocampal neurons and LPS-induced BV2 microglia cells. Models of TBI were established using controlled cortical impact (CCI) in vivo. CCK-8 assay, qRT-PCR and ELISA were used. Western blot was performed to assess the expression of CBS, CSE, IGF-1, and GHRH. Moreover, the recovery of TBI mice was evaluated for behavioral function by applying the modified Neurological Severity Score (mNSS), the Rotarod test, and the Morris water maze. Results: We discovered that serum H2S, CSF H2S, and serum IGF-1 concentrations were all adversely associated with the severity of the TBI, while the concentrations of IGF-1 and GH in CSF and GH in the serum were all positively related to TBI severity. Experiments in vitro and in vivo indicated that activated-BV2 cells enhanced the production of inflammatory cytokines and suppressed the cell viability of HT22 cells. In addition, treatment with NaHS, IGF-1, and GH alleviated the activation of BV2 cells. Furthermore, NaHS, IGF-1, and GH treatment alleviated motor function deficits after TBI. Conclusion: This study gives novel information on the functions of H2S, IGF-1, and GH in TBI.

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