Neuroprotective effects of hydrogen sulfide and the underlying signaling pathways

Chen, Wenlin; Niu, Yingying; Jiang, Wei-Zheng; Tang, Hui-Lan; Zhang, Chong; Xia, Qiming; Tang, Xiao‐Qing

doi:10.1515/revneuro-2014-0051

Cited by 56 publications

(34 citation statements)

References 27 publications

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“…TAA administration induces ALF, leading to cognitive deficiency and hepatic dysfunction in mice (17,24). Previous studies have provided evidence that endogenous H 2 S exerts a series of protective effects on the brain and liver (25)(26)(27). The aim of the present study was to investigate the role of H 2 S treatment in TAA-induced mouse models of ALF where the potential therapeutic value of H 2 S in this mouse model was also evaluated.…”

Section: Discussionmentioning

confidence: 97%

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Yuan

Huang

et al. 2020

Exp Ther Med

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Acute liver failure (ALF) is a devastating clinical syndrome with a high mortality rate if not treated promptly. Previous studies have demonstrated the beneficial effects of hydrogen sulfide (H 2 S) on the brain and liver. The present study aimed to investigate the potential protective effects of H 2 S in ALF. A mouse model of ALF was established following treatment with thioacetamide (TAA). Mice with TAA-induced ALF were intraperitoneally injected with 30 or 100 µmol/kg/day sodium hydrosulfide (NaHS; a H 2 S donor drug) for two weeks. According to results from novel object recognition and Y-maze tests, in the present study, NaHS treatment alleviated cognitive deficiency and preserved spatial orientation learning ability in TAA-induced ALF mice compared with those of untreated mice. In addition, NaHS treatment reduced serum levels of aspartate transaminase (AST), alanine transaminase (ALT) and the concentration of ammonia compared with those that received control treatment, resulting in weight loss prevention. These findings suggested a beneficial effect of H 2 S on liver function. In conclusion, results from the present study suggested that H 2 S treatment may alleviate cognitive deficiency and hepatic dysfunction in mice with ALF, indicating the potential therapeutic benefits of applying H 2 S for the treatment of ALF.

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Section: Discussionmentioning

confidence: 97%

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Yuan

Huang

et al. 2020

Exp Ther Med

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“…A protective effect on neuronal cells and also an activation of primary afferent neurons by soluble H 2 S have been reported, making H 2 S worthy of consideration as a new neurotransmitter [82]. …”

Section: Hydrogen Sulfide (H2s)mentioning

confidence: 99%

Anti-inflammatory effects of H2S during acute bacterial infection: a review

et al. 2017

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Hydrogen sulfide (H2S), previously only considered a toxic environmental air pollutant, is now increasingly recognized as an important signaling molecule able to modulate several cellular pathways in many human tissues. As demonstrated in recent studies, H2S is produced endogenously in response to different cellular stimuli and plays different roles in controlling a number of physiological responses. The precise role of H2S in inflammation is still largely unknown. In particular, the role of H2S in the regulation of the inflammatory response in acute and chronic infections is being actively investigated because of its potential therapeutic use. To study the effect of H2S as an anti-inflammatory mediator during bacterial infections, we developed an ex vivo model of primary cells and cell lines infected with Mycoplasma. Our data demonstrate a dichotomic effect of H2S on the NF-kB and Nrf-2 molecular pathways, which were inhibited and stimulated, respectively.

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“…1A, the doses of NaHS from 100 to 1,600 µmol/l markedly promoted cells proliferation, leading to an increase in cell viability and reaching a peaking at 400 µmol/l. Therefore, 400 µmol/l NaHS was used in the subsequent timeresponse study with different treatment times (12,24,36,48 and 60 h). As shown in Fig.…”

Section: Nahs Promotes Cell Proliferation In C6 Glioma Cellsmentioning

confidence: 99%

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

et al. 2015

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Abstract. Hydrogen sulfide (H 2 S) participates in multifarious physiological and pathophysiologic progresses of cancer both in vitro and in vivo.We have previously demonstrated that exogenous H 2 S promoted liver cancer cells proliferation/anti-apoptosis/angiogenesis/migration effects via amplifying the activation of NF-κB pathway. However, the effects of H 2 S on cancer cell proliferation and apoptosis are controversial and remain unclear in C6 glioma cells. The present study investigated the effects of exogenous H 2 S on cancer cells growth via activating p38 MAPK/ERK1/2-COX-2 pathways in C6 glioma cells. C6 glioma cells were treated with 400 µmol/l NaHS (a donor of H 2 S) for 24 h. The expression levels of phosphorylated (p)-p38 MAPK, total (t)-p38 MAPK, p-ERK1/2, t-ERK1/2, cyclooxygenase-2 (COX-2) and caspase-3 were measured by western blotting assay. Cell viability was detected by Cell Counting . Apoptotic cells were observed by Hoechst 33258 staining assay. Cell proliferation was directly detected under fully automatic inverted microscope. Exposure of C6 glioma cells to NaHS resulted in cell proliferation, as evidenced by an increase in cell viability. In addition, NaHS treatment reduced apoptosis, as indicated by the decreased apoptotic percentage and the cleaved caspase-3 expression. Importantly, exposure of the cells to NaHS increased the expression levels of p-p38 MAPK, p-ERK1/2 and COX-2. Notably, co-treatment of C6 glioma cells with 400 µmol/l NaHS and AOAA (an inhibitor of CBS) largely suppressed the above NaHS-induced effects. Combined treatment with NaHS and SB203580 (an inhibitor of p38 MAPK) or PD-98059 (an inhibitor of ERK1/2) resulted in the synergistic reduction of COX-2 expression and increase of caspase-3 expression, a decreased number of apoptotic cells, along with decreased cell viability. Combined treatment with NS-398 (an inhibitor of COX-2) and NaHS also resulted in the synergistic increase of caspase-3, a decreased in the number of apoptotic cells and the decrease in cell viability. The findings of the present study provide novel evidence that p38 MAPK/ERK1/2-COX-2 pathways are involved in NaHS-induced cancer cell proliferation and anti-apoptosis in C6 glioma cells.

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Neuroprotective effects of hydrogen sulfide and the underlying signaling pathways

Abstract: AbstractHydrogen sulfide (H

Cited by 56 publications

References 27 publications

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Hydrogen sulfide alleviates cognitive deficiency and hepatic dysfunction in a mouse model of acute liver failure

Anti-inflammatory effects of H2S during acute bacterial infection: a review

Exogenous hydrogen sulfide promotes C6 glioma cell growth through activation of the p38 MAPK/ERK1/2-COX-2 pathways

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