Open Access

Hyperforin improves post-stroke social isolation‑induced exaggeration of PSD and PSA via TGF-β

  • Authors:
    • Yujing Zhang
    • Peiyun Yu
    • Hong Liu
    • Hua Yao
    • Shanglong Yao
    • Shi‑Ying Yuan
    • Jian‑Cheng Zhang
  • View Affiliations

  • Published online on: November 2, 2018     https://doi.org/10.3892/ijmm.2018.3971
  • Pages: 413-425
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Stroke survivors often experience social isolation, which can lead to post‑stroke depression (PSD) and post‑stroke anxiety (PSA) that can compromise neurogenesis and impede functional recovery following the stroke. The present study aimed to investigate the effects and mechanisms of post‑stroke social isolation‑mediated PSD and PSA on hippocampal neurogenesis and cognitive function. The effects of the natural antidepressant hyperforin on post‑stroke social isolation‑mediated PSD and PSA were also investigated. In the present study, a model of PSD and PSA using C57BL/6J male mice was successfully established using middle cerebral artery occlusion combined with post‑stroke isolated housing conditions. It was observed that PSD and PSA were more prominent in the isolated mice compared with the pair‑housed mice at 14 days post‑ischemia (dpi). Mice isolated 3 dpi exhibited decreased transforming growth factor‑β (TGF‑β) levels and impairment of hippocampal neurogenesis and memory function at 14 dpi. Intracerebroventricular administration of recombinant TGF‑β for 7 consecutive days, starting at 7 dpi, restored the reduced hippocampal neurogenesis and memory function induced by social isolation. Furthermore, intranasal administration of hyperforin for 7 consecutive days starting at 7 dpi improved PSD and PSA and promoted hippocampal neurogenesis and memory function in the isolated mice at 14 dpi. The inhibition of TGF‑β with a neutralizing antibody prevented the effects of hyperforin. In conclusion, the results revealed a previously uncharacterized role of hyperforin in improving post‑stroke social isolation‑induced exaggeration of PSD and PSA and, in turn, promoting hippocampal neurogenesis and cognitive function via TGF‑β.
View Figures
View References

Related Articles

Journal Cover

January 2019
Volume 43 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
APA
Zhang, Y., Yu, P., Liu, H., Yao, H., Yao, S., Yuan, S., & Zhang, J. (2019). Hyperforin improves post-stroke social isolation‑induced exaggeration of PSD and PSA via TGF-β. International Journal of Molecular Medicine, 43, 413-425. https://doi.org/10.3892/ijmm.2018.3971
MLA
Zhang, Y., Yu, P., Liu, H., Yao, H., Yao, S., Yuan, S., Zhang, J."Hyperforin improves post-stroke social isolation‑induced exaggeration of PSD and PSA via TGF-β". International Journal of Molecular Medicine 43.1 (2019): 413-425.
Chicago
Zhang, Y., Yu, P., Liu, H., Yao, H., Yao, S., Yuan, S., Zhang, J."Hyperforin improves post-stroke social isolation‑induced exaggeration of PSD and PSA via TGF-β". International Journal of Molecular Medicine 43, no. 1 (2019): 413-425. https://doi.org/10.3892/ijmm.2018.3971