Open Access

Salsolinol improves angiotensin II‑induced myocardial fibrosis in vitro via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway

  • Authors:
    • Xian Zhang
    • Ze Shao
    • Yuchao Ni
    • Feilong Chen
    • Xia Yu
    • Jiasheng Wen
  • View Affiliations

  • Published online on: September 27, 2023     https://doi.org/10.3892/etm.2023.12226
  • Article Number: 527
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The clinical incidence of congestive heart failure (CHF) is very high and it poses a significant threat to the health of patients. The traditional Chinese medicine monomer salsolinol is widely used to treat similar symptoms of CHF. However, there have been no reports on the effect of salsolinol for the management of CHF and its effects on myocardial fibrosis. In the present study, salsolinol was used to treat angiotensin II (AngII)‑induced human cardiac fibroblasts (HCFs) and cell proliferation and migration were assessed using a CCK‑8, EdU staining assay and wound healing assay. Subsequently, immunofluorescence, western blotting and other techniques were used to detect indicators associated with cell fibrosis and relevant kits were used to detect markers of cellular inflammation and reactive oxygen species (ROS) production. Molecular docking analysis was used to predict the relationship between salsolinol and lysine‑specific histone demethylase 1A (LSD1). Subsequently, the expression of LSD1 in the serum of CHF patients was detected by reverse transcription‑quantitative PCR. Finally, LSD1 was overexpressed in cells to explore the regulatory mechanism of salsolinol in AngII‑induced HFCs. Salsolinol reduced the proliferation and migration. Salsolinol reduced the expression of fibrosis marker proteins α‑smooth muscle actin, Collagen I and Collagen III in a concentration‑dependent manner, thereby reducing cell fibrosis. In addition, salsolinol reduced the levels of TNF‑α and IL‑6 in the cell supernatant and ROS production following AngII induction. Salsolinol inhibited LSD1 expression and regulated the STAT3/Notch‑1 signaling pathway. Upregulation of LSD1 reversed the effects of salsolinol on AngII‑induced HCFs. Salsolinol inhibited LSD1 via regulation of the STAT3/Notch‑1 signaling pathway to improve Ang II‑induced myocardial fibrosis in vitro.
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November-2023
Volume 26 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhang X, Shao Z, Ni Y, Chen F, Yu X and Wen J: Salsolinol improves angiotensin II‑induced myocardial fibrosis <em>in vitro</em> via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway. Exp Ther Med 26: 527, 2023
APA
Zhang, X., Shao, Z., Ni, Y., Chen, F., Yu, X., & Wen, J. (2023). Salsolinol improves angiotensin II‑induced myocardial fibrosis <em>in vitro</em> via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway. Experimental and Therapeutic Medicine, 26, 527. https://doi.org/10.3892/etm.2023.12226
MLA
Zhang, X., Shao, Z., Ni, Y., Chen, F., Yu, X., Wen, J."Salsolinol improves angiotensin II‑induced myocardial fibrosis <em>in vitro</em> via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway". Experimental and Therapeutic Medicine 26.5 (2023): 527.
Chicago
Zhang, X., Shao, Z., Ni, Y., Chen, F., Yu, X., Wen, J."Salsolinol improves angiotensin II‑induced myocardial fibrosis <em>in vitro</em> via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway". Experimental and Therapeutic Medicine 26, no. 5 (2023): 527. https://doi.org/10.3892/etm.2023.12226