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.