Pathophysiological Concepts in Multiple Sclerosis and the Therapeutic Effects of Hydrogen Sulfide

Talaei, Fatemeh

doi:10.15412/j.bcn.03070206

Cited by 8 publications

(13 citation statements)

References 69 publications

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“…H2S upregulated proteins involved in immune system response and downregulated PBMNCs- and EC-related adhesion molecules (LFA-1 and VCAM-1) [127]. Furthermore, it had a cell expansion-inducing effect, altering EC morphology.…”

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

“…Furthermore, it had a cell expansion-inducing effect, altering EC morphology. The effects of H2S on OPCs and astrocytes were studied compared to mTOR inhibitor rapamycin [127]. In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production [127].…”

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

“…The effects of H2S on OPCs and astrocytes were studied compared to mTOR inhibitor rapamycin [127]. In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production [127]. NaHS slowed but did not inhibit the differentiation of OCPs or the production of myelin compared to rapamycin [127].…”

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

“…In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production [127]. NaHS slowed but did not inhibit the differentiation of OCPs or the production of myelin compared to rapamycin [127]. Thus these data suggest that H2S may provide potential therapeutic application against MS.…”

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

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Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration

Sen

2017

Journal of Molecular Biology

128

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Hydrogen sulfide (H2S) a novel gasotransmitter is endogenously synthesized by multiple enzymes that are differentially expressed in the peripheral tissues and central nervous systems. H2S regulates a wide range of physiological processes ranging from cardiovascular, neuronal, immune, respiratory, gastrointestinal, liver, and endocrine systems by influencing cellular signaling pathways and sulfhydration of target proteins. This review focuses on the recent progress made in H2S signaling that affects mechanistic and functional aspects of several biological processes such as autophagy, inflammation, proliferation and differentiation of stem cell, cell survival/death, and cellular metabolism under both physiological and pathological conditions. Moreover we highlighted the crosstalk between nitric oxide (NO) and H2S in several bilogical contexts.

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Section: Inflammation and H2s Signalingmentioning

confidence: 99%

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

Section: Inflammation and H2s Signalingmentioning

confidence: 99%

See 2 more Smart Citations

Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration

Sen

2017

Journal of Molecular Biology

128

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“…It has been suggested that H 2 S exerts neuroprotective effects in neuroinflammatory diseases, including neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, and stroke, and autoimmune diseases of the central nervous system (CNS), such as multiple sclerosis [ 3 , 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

The H2S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide

et al. 2018

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GYY4137 is a hydrogen sulfide (H2S) donor that has been shown to act in an anti-inflammatory manner in vitro and in vivo. Microglial cells are among the major players in immunoinflammatory, degenerative, and neoplastic disorders of the central nervous system, including multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and glioblastoma multiforme. So far, the effects of GYY4137 on microglial cells have not been thoroughly investigated. In this study, BV2 microglial cells were stimulated with interferon-gamma and lipopolysaccharide and treated with GYY4137. The agent did not influence the viability of BV2 cells in concentrations up to 200 μM. It inhibited tumor necrosis factor but not interleukin-6 production. Expression of CD40 and CD86 were reduced under the influence of the donor. The phagocytic ability of BV2 cells and nitric oxide production were also affected by the agent. Surprisingly, GYY4137 upregulated generation of reactive oxygen species (ROS) by BV2 cells. The effect was mimicked by another H2S donor, Na2S, and it was not reproduced in macrophages. Our results demonstrate that GYY4137 downregulates inflammatory properties of BV2 cells but increases their ability to generate ROS. Further investigation of this unexpected phenomenon is warranted.

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Hydrogen Sulphide-Based Therapeutics for Neurological Conditions: Perspectives and Challenges

et al. 2023

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Central nervous system (CNS)-related conditions are currently the leading cause of disability worldwide, posing a significant burden to health systems, individuals and their families. Although the molecular mechanisms implicated in these disorders may be varied, neurological conditions have been increasingly associated with inflammation and/or impaired oxidative response leading to further neural cell damages. Therefore, therapeutic approaches targeting these defective molecular mechanisms have been vastly explored. Hydrogen sulphide (H2S) has emerged as a modulator of both inflammation and oxidative stress with a neuroprotective role, therefore, has gained interest in the treatment of neurological disorders. H2S, produced by endogenous sources, is maintained at low levels in the CNS. However, defects in the biosynthetic and catabolic routes for H2S metabolism have been identified in CNS-related disorders. Approaches to restore H2S availability using H2S-donating compounds have been recently explored in many models of neurological conditions. Nonetheless, we still need to elucidate the potential for these compounds not only to ameliorate defective biological routes, but also to better comprehend the implications on H2S delivery, dosage regimes and feasibility to successfully target CNS tissues. Here, we highlight the molecular mechanisms of H2S-dependent restoration of neurological functions in different models of CNS disease whilst summarising current administration approaches for these H2S-based compounds. We also address existing barriers in H2S donor delivery by showcasing current advances in mediating these constrains through novel biomaterial-based carriers for H2S donors.

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Pathophysiological Concepts in Multiple Sclerosis and the Therapeutic Effects of Hydrogen Sulfide

Cited by 8 publications

References 69 publications

Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration

Functional and Molecular Insights of Hydrogen Sulfide Signaling and Protein Sulfhydration

The H2S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide

Hydrogen Sulphide-Based Therapeutics for Neurological Conditions: Perspectives and Challenges

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