Abstract
Background and Aims: Cognitive impairment is one of the major complications of subarachnoid hemorrhage (SAH) and is closely associated with neuroinflammation. Hydrogen sulfide (H2S) has been shown to have an anti-inflammatory effect and reduce cognitive impairment in neurodegenerative diseases, but its effects in SAH have been little studied. This study aimed to investigate the effects of H2S on cognitive impairment after SAH and the possible underlying mechanisms.Methods: Forty-eight male Sprague–Dawley (SD) rats were randomly divided into three groups: a sham group, a SAH group, and a SAH + NaHS (an H2S donor) group. The endovascular perforation technique was used to establish the experimental SAH model. NaHS was administered intraperitoneally. An active avoidance test (AAT) was performed to investigate cognitive function. The expression of TNF-α, toll-like receptor 4 (TLR4), and NF-κB p65 in the hippocampus was measured by Western blot and immunohistochemistry. The types of cells expressing TNF-α were detected by double immunofluorescence staining.Results: Compared to that in the sham group, the learning and memory ability of rats in the SAH group was damaged. Furthermore, the expression of TNF-α, TLR4, and NF-κB p65 in the hippocampus was elevated in the SAH group (p < 0.05). TNF-α was mainly expressed in activated microglia, which was consistent with the expression of TLR4. Treatment with NaHS significantly decreased the cognitive impairment of rats after SAH and simultaneously reduced the expression of TNF-α, TLR4, and NF-κB p65 and alleviated the nuclear translocation of NF-κB p65 (p < 0.05).Conclusions: The neuroinflammation reaction in microglia contributes to cognitive impairment after SAH. H2S reduced the cognitive impairment of rats after SAH by ameliorating neuroinflammation in microglia, potentially via the TLR4/NF-κB pathway.
Highlights
Subarachnoid hemorrhage (SAH) accounts for 5–9% of all strokes but is responsible for 30% of stroke-related mortality (El Amki et al, 2018) and affects people younger than those who suffer ischemic strokes
This study investigated the hypothesis that H2S can reduce cognitive impairment after SAH, potentially by ameliorating neuroinflammation mediated by the toll-like receptor 4 (TLR4)/NF-κB pathway in the brain
The neurological scores and motor function scores of rats at 24 h after surgery were significantly lower in the SAH group than in the sham group, suggesting pronounced neurological impairment induced by SAH
Summary
Subarachnoid hemorrhage (SAH) accounts for 5–9% of all strokes but is responsible for 30% of stroke-related mortality (El Amki et al, 2018) and affects people younger than those who suffer ischemic strokes. One of the major complications of SAH, mainly manifests as dysfunctions of memory, executive function, and language (Etminan and Macdonald, 2017). TLRs play crucial roles in the innate immune system by recognizing pathogenassociated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) and lead to activation of the NF-κB transcription factors. These transcription factors regulate the expression of cytokines and chemokines such as TNF-α (Kawasaki and Kawai, 2014). Cognitive impairment is one of the major complications of subarachnoid hemorrhage (SAH) and is closely associated with neuroinflammation. This study aimed to investigate the effects of H2S on cognitive impairment after SAH and the possible underlying mechanisms
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