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  2. Salidroside Ameliorates Ischemia/Reperfusion-Induced Human Cardiomyocyte Injury by Inhibiting the Circ_0097682/miR-671-5p/USP46 Pathway

Salidroside Ameliorates Ischemia/Reperfusion-Induced Human Cardiomyocyte Injury by Inhibiting the Circ_0097682/miR-671-5p/USP46 Pathway

  • Cardiovasc Toxicol. 2023 Sep 22. doi: 10.1007/s12012-023-09808-3.
Yuyang Yang 1 Fangqian Liang 2 Jingyuan Gao 3 Jian Li 1 Chunhua Jiang 1 Wei Xie 1 Shujuan Wu 1 Ya Wang 1 Jing Yi 1
Affiliations

Affiliations

  • 1 College of Traditional Chinese Medicine, North China University of Science Technology, Qinhuangdao, China.
  • 2 Department of General Practice, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Lubei District, Tangshan, 063000, Hebei, China.
  • 3 Department of General Practice, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Lubei District, Tangshan, 063000, Hebei, China. gaojingyuan2009@126.com.
Abstract

Salidroside shows an inhibitory effect on myocardial ischemia/reperfusion (I/R) injury; however, the underlying mechanism remains to be explored. The present work analyzes the mechanism that drives salidroside to ameliorate I/R-induced human cardiomyocyte injury. Human cardiomyocytes were subjected to I/R treatment to simulate a myocardial infarction cell model. Cell viability, cell proliferation, and cell Apoptosis were analyzed by CCK-8 assay, EdU assay, and flow cytometry analysis, respectively. RNA expression levels of circ_0097682, miR-671-5p, and F-box and Ubiquitin-Specific Peptidase 46 (USP46) were detected by qRT-PCR. Protein expression was measured by Western blotting assay. The levels of IL-6, IL-1β, and TNF-α in cell supernatant were detected by enzyme-linked immunosorbent assays. Salidroside treatment relieved I/R-induced inhibitory effect on AC16 cell proliferation and promoting effects on cell Apoptosis, inflammation, and oxidative stress. Salidroside inhibited circ_0097682 expression in I/R-treated AC16 cells. Salidroside-mediated inhibition of I/R-induced cell injury involved the downregulation of circ_0097682 expression. In addition, circ_0097682 bound to miR-671-5p in AC16 cells, and miR-671-5p inhibitors rescued salidroside pretreatment-mediated effects in I/R-treated AC16 cells. Moreover, miR-671-5p targeted USP46 in AC16 cells, and USP46 introduction partially relieved circ_0097682 depletion or salidroside pretreatment-induced effects in I/R-treated AC16 cells. Salidroside ameliorated I/R-induced AC16 cell injury by inhibiting the circ_0097682/miR-671-5p/USP46 pathway.

Keywords

AC16 cells; Injury; Myocardial ischemia/reperfusion injury; Salidroside; circ_0097682.

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