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Background and purpose <p>Traumatic brain injury (TBI) is a multifaceted pathological condition affecting people worldwide. Hydrogen sulfide (H<sub>2</sub>S) is a newly identified gaseous mediator and is testified to be beneficial in various conditions of physiology and pathology. Following TBI, the regulation of H<sub>2</sub>S is disrupted. Sodium hydrogen sulfide (NaHS) functions effectively as a source of H<sub>2</sub>S. It functions against neuroinflammation in different neurological conditions, including injury, relieving the cascades of secondary injury processes. However, it has not been exploited to mitigate the adverse effects of TBI-induced glial activation, potentially by restoring the balance of H<sub>2</sub>S synthesis and degradation.</p> Experimental approach <p>We developed a weight-drop model of TBI to establish the effects of NaHS treatment. We validated our findings by behavioral tasks, estimated H<sub>2</sub>S levels by fluorescent probe, quantitatively measured H<sub>2</sub>S-synthesizing and degrading enzymes by immunoblotting, and analyzed the morphology of astrocytes and microglia by immunofluorescence.</p> Key results <p>We found that NaHS treatment restored the H<sub>2</sub>S levels by upregulating H<sub>2</sub>S- synthesizing and downregulating H<sub>2</sub>S-degrading enzymes post-TBI. It also mitigated TBI-induced neuroinflammation as depicted by the altered morphology of astrocytes and microglia. The reasons for such modifications were credited to the altered phosphorylation status of different kinases that facilitate the functions of many downstream signaling molecules in the S100β/RSK1 and RAS/RAF/MEK/ERK/NF-κB pathways.</p> Conclusion and implications <p>The data gathered here suggest that NaHS could work well as a potential therapeutic agent against TBI-induced brain pathology, ameliorating astrocyte and microglia activation owing to alterations of proteins involved in H<sub>2</sub>S synthesis and degradation.</p> Graphical abstract <p></p>

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Sodium hydrogen sulfide restores H2S-synthesizing and degrading enzymes to alleviate glial activation after traumatic brain injury in male mice

  • 期刊论文

  • 发表日期：

    2025年10月2日

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  • Farheen Nasir,
  • Priyanka Yadav,
  • Thamil Mani Sivanandam

摘要

Background and purpose

Traumatic brain injury (TBI) is a multifaceted pathological condition affecting people worldwide. Hydrogen sulfide (H2S) is a newly identified gaseous mediator and is testified to be beneficial in various conditions of physiology and pathology. Following TBI, the regulation of H2S is disrupted. Sodium hydrogen sulfide (NaHS) functions effectively as a source of H2S. It functions against neuroinflammation in different neurological conditions, including injury, relieving the cascades of secondary injury processes. However, it has not been exploited to mitigate the adverse effects of TBI-induced glial activation, potentially by restoring the balance of H2S synthesis and degradation.

Experimental approach

We developed a weight-drop model of TBI to establish the effects of NaHS treatment. We validated our findings by behavioral tasks, estimated H2S levels by fluorescent probe, quantitatively measured H2S-synthesizing and degrading enzymes by immunoblotting, and analyzed the morphology of astrocytes and microglia by immunofluorescence.

Key results

We found that NaHS treatment restored the H2S levels by upregulating H2S- synthesizing and downregulating H2S-degrading enzymes post-TBI. It also mitigated TBI-induced neuroinflammation as depicted by the altered morphology of astrocytes and microglia. The reasons for such modifications were credited to the altered phosphorylation status of different kinases that facilitate the functions of many downstream signaling molecules in the S100β/RSK1 and RAS/RAF/MEK/ERK/NF-κB pathways.

Conclusion and implications

The data gathered here suggest that NaHS could work well as a potential therapeutic agent against TBI-induced brain pathology, ameliorating astrocyte and microglia activation owing to alterations of proteins involved in H2S synthesis and degradation.

Graphical abstract