Novel neuroprotective role of hydrogen sulfide in a rat model of stress brain injury

Elbassuoni, Eman; Nazmy, Walaa H.

doi:10.4149/gpb_2017029

Cited by 6 publications

(5 citation statements)

References 67 publications

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“…The significant increase in iNOS levels with XE exposure observed in the current study can be explained by the significant increase of iNOS level that in turn increased NO production in rats exposed to XE in comparison with control and NaHS groups and this result is in agreement with previous studies (Saber et al, 2019). The overexpression of NO with stress results in formation of reactive nitrogen species that is considered to be one of the leading causes of injury with stress exposure (Elbassuoni and Nazmy, 2018) and as found in the present study.…”

Section: -Discussionsupporting

confidence: 92%

“…H2S can limit ROS either by directly scavenging free radicals, thus regulating oxidative signaling pathways, or by suppressing the inflammatory response (Stein and Bailey, 2013). The inducible nitric oxide synthase (iNOS) is scarcely present normally but can be expressed during immunological challenge and stress (Elbassuoni and Nazmy, 2018). The significant increase in iNOS levels with XE exposure observed in the current study can be explained by the significant increase of iNOS level that in turn increased NO production in rats exposed to XE in comparison with control and NaHS groups and this result is in agreement with previous studies (Saber et al, 2019).…”

Section: -Discussionmentioning

confidence: 99%

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The potential anti-inflammatory and anti-apoptotic influence of hydrogen sulfide on xenoestrogen induced-toxicity in rats

Hassan

2023

Benha Veterinary Medical Journal

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Hydrogen sulphide (H2S) is a gas transmitter that plays a vital role in a variety of physiological and pathological processes. Xenoestrogen (XE) a regularly used manufacturing chemical, has been related to endocrine disruptor. The purpose of this study was to investigate the effects of H2S donor (sodium hydrogen sulfide [NaHS]) on xenoestrogen (XE)-induced toxicity in rats. Twenty-four adult female rats were divided into three groups (8 rats /group): group I: control group, group II: rats were intraperitoneally (IP) injected with XE (150 mg/kg body weight/ day) dissolved in corn oil for 4 weeks, group III: rats were IP injected with H2S donor NaHS intraperitoneally (IP) at daily dose of 5 mg/kg body weight/day dissolved in deionized water for 6 weeks and were injected with XE as group II. Biomarkers including lactate dehydrogenase (LDH), Interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), hypoxia-inducible factor 1 alpha (HIF 1α), caspase-3 were determined and lymphocytes %. The obtained results revealed that; in group 3, a significant decrease in serum LDH, lymphocytes %, iNOS, with marked decrease in serum Caspase-3 when compared to group II. These results suggests that H2S might ameliorate XE inducedtoxicity via its anti-inflammatory and anti-apoptotic effects.

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Section: -Discussionsupporting

confidence: 92%

Section: -Discussionmentioning

confidence: 99%

The potential anti-inflammatory and anti-apoptotic influence of hydrogen sulfide on xenoestrogen induced-toxicity in rats

Hassan

2023

Benha Veterinary Medical Journal

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“…Hydrogen sulfide (H 2 S), the third gasotransmitter after carbon monoxide (CO) and nitric oxide (NO) (Wang, 2010), exerts protective effect in the CNS (Zhang and Bian, 2014;Panthi et al, 2016;Elbassuoni and Nazmy, 2018). Emerging evidence has indicated that H 2 S has anti-oxidative, anti-ER stress, and antiapoptotic properties in the CNS (Jiang et al, 2011;Nie et al, 2013;Li et al, 2014;.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

Zuo

Jiang

et al. 2020

Front. Neurosci.

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Sleep deprivation (SD) induces hippocampal damage. Hydrogen sulfide (H 2 S) is a neuronal protective factor. Silence information regulating factor 1 (Sirt1) plays an important role in neuroprotection. Therefore, this study was aimed at exploring whether H 2 S meliorates SD-induced hippocampal damage and whether Sirt1 mediates this protective role of H 2 S. We found that sodium hydrosulfide (NaHS, a donor of H 2 S) alleviated SD-generated hippocampal oxidative stress, including increases in the activation of SOD and the level of GSH as well as a decrease in the level of MDA. Meanwhile, we found that NaHS reduced SD-exerted hippocampal endoplasmic reticulum (ER) Stress, including downregulations of GRP78, CHOP, and cleavedcaspase-12 expression. Moreover, NaHS reduced the apoptosis in the SD-exposed hippocampus, and this included decreases in the number of apoptotic cells and the activation of caspase-3, downregulation of Bax expression, and upregulation of Bcl-2 expression. NaHS upregulated the expression of Sirt1 in the hippocampus of SDexposed rats. Furthermore, Sirtinol, the inhibitor of Sirt1, abrogated the protection of NaHS against SD-exerted hippocampal oxidative stress, ER stress, and apoptosis. These results suggested that H 2 S alleviates SD-induced hippocampal damage by upregulation of hippocampal Sirt1.

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“…Newborns diagnosed with asphyxia at birth and followed up to 2 years of age, saw that lesions in neuronal structures generated in the prenatal period, are possible to be identified right at birth, within 24 h postnatal [49]. Additionally, a study that evaluated the effect of hydrogen sulfide in a model of brain injury by stress in rats, identified an increase in serum NSE levels, as well as an increase in the levels of ROS and reactive nitrogen species (RNS), causing oxidative stress [51]. In the maternal exposure to infections or inflammations in the prenatal period, an increase in NSE in the offspring was found previously.…”

Section: Discussionmentioning

confidence: 99%

6-Shogaol Exerts a Neuroprotective Factor in Offspring after Maternal Immune Activation in Rats

Rosa¹,

Medeiros²,

Oliveira³

et al. 2021

Dev Neurosci

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6-Shogaol is one of the main active phenolic components of ginger and has neuroprotective effects by protecting brain against the oxidative stress and regulate the levels of neurotrophic factors. The objective of the present study was to verify the effect of 6-shogaol on neurochemical parameters in offspring after maternal immune activation by lipopolysaccharide (LPS) in rats. Twelve pregnant Wistar rats received 100 μg/kg of LPS or saline solution on the gestational day 9.5. Male offspring participated in the study and from the postnatal days (PND) 30 and 55, respectively, they were supplemented with 6-shogaol or saline solution, by gavage at a dose of 10 mg/kg/day, orally for 5 days. In PND 37 and 62, analysis of kinase signaling regulated by extracellular signal 1/2 (ERK 1/2), levels of neurotrophic factor derived from the brain (BDNF), and neuron-specific enolase (NSE), lipid and protein oxidative damage was evaluated by 4-hydroxy-2-nonenal (HNE) and 3-nitrotyrosine (3-NT), respectively, and myeloperoxidase (MPO) activity was performed in the hippocampus. Prenatal exposure to LPS significantly decreased ERK and BDNF levels in PND 37 and 62, increased NSE levels and lipid damage in rats in PND 37, and increased 3-NT level in rats in PND 62. With treatment using 6-shogaol, an increase in ERK and BDNF levels was identified in PND 37 and 62 and a reduction in HNE and MPO activity in rats in PND 37 and 62, respectively. 6-Shogaol positively increased markers of neuronal growth, plasticity and synaptic activity and reduced oxidative damage in the hippocampus in an animal model of autism by maternal immune activation.

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Novel neuroprotective role of hydrogen sulfide in a rat model of stress brain injury

Cited by 6 publications

References 67 publications

The potential anti-inflammatory and anti-apoptotic influence of hydrogen sulfide on xenoestrogen induced-toxicity in rats

The potential anti-inflammatory and anti-apoptotic influence of hydrogen sulfide on xenoestrogen induced-toxicity in rats

Hydrogen Sulfide Prevents Sleep Deprivation-Induced Hippocampal Damage by Upregulation of Sirt1 in the Hippocampus

6-Shogaol Exerts a Neuroprotective Factor in Offspring after Maternal Immune Activation in Rats

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