Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure

Mohseni, Fahimeh; Bagheri, Farzaneh; Rafaiee, Raheleh; Norozi, Pirasteh; Khaksari, Mehdi

doi:10.1016/j.physbeh.2019.112784

Cited by 10 publications

(3 citation statements)

References 43 publications

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“…In this study, mineralocorticoid receptor antagonists also restored the levels of H 2 S in the frontal cortex and hippocampus regions in Aβ‐injected mice suggesting the possible role of H 2 S in cognition improving actions. H 2 S is a gaseous neurotransmitter, and its memory improving actions have been reported [52]. Furthermore, the administration of ANA‐12 (BDNF antagonist) ameliorated the aldosterone‐antagonist‐mediated increase in the levels of H 2 S suggesting the possible interrelationship between BDNF and H 2 S in aldosterone‐mediated beneficial actions.…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling

Chen

Shi

She

et al. 2020

Fundamemntal Clinical Pharma

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The present study explored the role and mechanisms of mineralocorticoid receptor antagonists in β‐amyloid (Aβ)‐induced cognitive impairment. A single intracerebroventricular injection of Aβ1‐42 was given to mice, and after 14 days of injection, memory was evaluated using the Morris water maze test. Spironolactone (25 and 50 mg/kg) and eplerenone (50 and 100 mg/kg) were administered for two days before and for 14 days after Aβ injection. Mineralocorticoid receptor blockers attenuated Aβ‐induced cognitive impairment assessed in terms of decrease in day 4 escape latency time (ELT) in comparison to day 1 ELT (suggesting an increase in learning) along with an increase in time spent in target quadrant on day 5 (suggesting the retrieval of learned things). These drugs also increased the expression of BDNF, H2S, Nrf2, reduced glutathione, and decreased β‐amyloid and TNF‐α in the frontal cortex and hippocampus. Co‐administration of ANA‐12, BDNF receptor antagonist (0.25 and 0.5 mg/kg) abolished cognitive improving functions of mineralocorticoid receptor blockers, attenuated H2S, Nrf2, reduced glutathione, and decreased β‐amyloid and TNF‐α. It is concluded that spironolactone and eplerenone attenuate cognitive decline of Alzheimer's type, possibly through upregulation of BDNF levels in the frontal cortex and hippocampus, which may increase H2S, decrease Aβ, activate Nrf2‐dependent antioxidant system, and decrease neuroinflammation.

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Section: Discussionmentioning

confidence: 99%

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling

Chen

Shi

She

et al. 2020

Fundamemntal Clinical Pharma

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“…It is known that H 2 S is able to modulate the level of neurotrophic factors in normal and pathological conditions [ 26 , 179 , 180 ]. Thus, in a mouse TBI model, the administration of an H 2 S donor restored GDNF and NGF levels in damaged neural tissue, preserving their neuroprotective effects [ 67 ].…”

Section: The Role Of H 2 S In Cell Death In Neurot...mentioning

confidence: 99%

The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases

Rodkin

Nwosu

Sannikov

et al. 2023

IJMS

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Injuries of the central (CNS) and peripheral nervous system (PNS) are a serious problem of the modern healthcare system. The situation is complicated by the lack of clinically effective neuroprotective drugs that can protect damaged neurons and glial cells from death. In addition, people who have undergone neurotrauma often develop mental disorders and neurodegenerative diseases that worsen the quality of life up to severe disability and death. Hydrogen sulfide (H2S) is a gaseous signaling molecule that performs various cellular functions in normal and pathological conditions. However, the role of H2S in neurotrauma and mental disorders remains unexplored and sometimes controversial. In this large-scale review study, we examined the various biological effects of H2S associated with survival and cell death in trauma to the brain, spinal cord, and PNS, and the signaling mechanisms underlying the pathogenesis of mental illnesses, such as cognitive impairment, encephalopathy, depression and anxiety disorders, epilepsy and chronic pain. We also studied the role of H2S in the pathogenesis of neurodegenerative diseases: Alzheimer’s disease (AD) and Parkinson’s disease (PD). In addition, we reviewed the current state of the art study of H2S donors as neuroprotectors and the possibility of their therapeutic uses in medicine. Our study showed that H2S has great neuroprotective potential. H2S reduces oxidative stress, lipid peroxidation, and neuroinflammation; inhibits processes associated with apoptosis, autophagy, ferroptosis and pyroptosis; prevents the destruction of the blood-brain barrier; increases the expression of neurotrophic factors; and models the activity of Ca2+ channels in neurotrauma. In addition, H2S activates neuroprotective signaling pathways in psychiatric and neurodegenerative diseases. However, high levels of H2S can cause cytotoxic effects. Thus, the development of H2S-associated neuroprotectors seems to be especially relevant. However, so far, all H2S modulators are at the stage of preclinical trials. Nevertheless, many of them show a high neuroprotective effect in various animal models of neurotrauma and related disorders. Despite the fact that our review is very extensive and detailed, it is well structured right down to the conclusions, which will allow researchers to quickly find the proper information they are interested in.

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“…Therefore, the inhibition of NF-κB pro-inflammatory signaling was proposed as the potential mechanism of anti-inflammatory effects of H 2 S upon alcohol and cigarette smoke exposure [ 121 ]. In addition, H 2 S was shown to increase hippocampal neurogenesis in a model of fetal alcohol disorders through the up-regulation of BrdU and BDNF expression in dentate gyrus area, in parallel with reduced apoptosis rate, altogether resulting in improved spatial memory [ 122 ].…”

Section: Exogenous Neurotoxicantsmentioning

confidence: 99%

Hydrogen Sulfide (H2S) Signaling as a Protective Mechanism against Endogenous and Exogenous Neurotoxicants

Aschner

Skalny

Tang

et al. 2022

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In view of significant role of H2S in brain functioning through, it is proposed that H2S may also possess protective effects against adverse effects of neurotoxicants. Therefore, the objective of the present review is discussion of neuroprotective effects of H2S against toxicity of a wide spectrum of endogenous and exogenous agents, involved in pathogenesis of neurological diseases as etiological factors or key players in disease pathogenesis. Generally, the existing data demonstrate that H2S possesses neuroprotective effects upon exposure to endogenous (amyloid β, glucose and advanced-glycation end-products, homocysteine, lipopolysaccharide, and ammonia) and exogenous (alcohol, formaldehyde, acrylonitrile, metals, 6-hydroxydopamine, as well as 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenyl pyridine ion (MPP) neurotoxicants. On the one hand, neuroprotective effects are mediated by S-sulfhydration of key regulators of antioxidant (Sirt1, Nrf2) and inflammatory response (NF-κB) resulting in modulation of the downstream signaling, such as SIRT1/TORC1/CREB/BDNF-TrkB, Nrf2/ARE/HO-1, or other pathways. On the other hand, H2S appears to possess direct detoxicative effect through binding of endogenous (ROS, AGEs, Aβ) and exogenous (MeHg) neurotoxicants, thus reducing their toxicity. Moreover, alteration of H2S metabolism through inhibition of H2S-synthetizing enzymes in brain (CBS, 3-MST) may be considered as a significant mechanism of neurotoxicity. Taken together, the existing data indicate that modulation of cerebral H2S metabolism may be used as a neuroprotective strategy to counteract neurotoxicity of a wide spectrum of endogenous and exogenous neurotoxicants associated with neurodegeneration (Alzheimer’s and Parkinson’s disease), fetal alcohol syndrome, hepatic encephalopathy, environmental neurotoxicant exposure, etc. In this particular case, modulation of H2S-synthetizing enzymes or the use of H2S-releasing drugs should be considered as the potential tools, although particular efficiency and safety of such interventions are to be addressed in further studies.

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Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure

Cited by 10 publications

References 43 publications

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling

The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases

Hydrogen Sulfide (H2S) Signaling as a Protective Mechanism against Endogenous and Exogenous Neurotoxicants

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Hydrogen sulfide improves spatial memory impairment via increases of BDNF expression and hippocampal neurogenesis following early postnatal alcohol exposure

Cited by 10 publications

References 43 publications

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H2S‐Nrf2 signaling

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H2S‐Nrf2 signaling

The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases

Hydrogen Sulfide (H2S) Signaling as a Protective Mechanism against Endogenous and Exogenous Neurotoxicants

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Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling

Mineralocorticoid receptor antagonist‐mediated cognitive improvement in a mouse model of Alzheimer's type: possible involvement of BDNF‐H₂S‐Nrf2 signaling