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Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway

  • Authors:
    • Zhe Tang
    • Yong Wang
    • Yan Liu
    • Chenglong Li
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First People's Hospital of Jing Zhou/The First Affiliated Hospital of Yangtze University, Jingzhou, Hubei 434000, P.R. China, Department of Urology, Ying Shan Hospital of Traditional Chinese Medicine, Ying Shan, Hubei 438700, P.R. China, Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
    Copyright: © Tang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 507
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    Published online on: September 14, 2023
       https://doi.org/10.3892/etm.2023.12206
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Abstract

Renal ischemia/reperfusion injury (RIRI) represents the principal factor underlying acute kidney injury (AKI), which primarily stems from cellular injuries and ferroptosis caused by reactive oxygen species (ROS). Salidroside (SA), an antioxidant natural ester, has been attributed with the potential to protect against RIRI. In the present study, rats received daily SA doses (1, 10, or 100 mg/kg) by gavage for 7 consecutive days before surgery. The results revealed aggravated renal injury in the RIRI group, which was effectively prevented by SA pretreatment (10 and 100 mg/kg), with the 1 mg/kg dosage demonstrating lesser efficacy. Additionally, the results indicated that SA pretreatment mitigated the RIRI‑related upregulation of antioxidative superoxide dismutase. In vitro studies corroborated SA's ability to maintain hypoxia/reoxygenation‑treated NRK cell viability, with the protective effect being observed at SA concentrations ≥1 µM and peaking at 100 µM. Furthermore, the results showed that SA safeguarded renal tubular epithelial cells from oxidative damage, reduced ROS accumulation, and inhibited ferroptosis via activation of the PI3K/AKT signaling pathway. Therefore, the results of the present study highlight the promising therapeutic potential of SA as an effective intervention for RIRI via targeting of PI3K/AKT signaling pathway‑mediated anti‑oxidative and anti‑ferroptotic mechanisms.
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Copy and paste a formatted citation
Spandidos Publications style
Tang Z, Wang Y, Liu Y and Li C: Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway. Exp Ther Med 26: 507, 2023.
APA
Tang, Z., Wang, Y., Liu, Y., & Li, C. (2023). Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway. Experimental and Therapeutic Medicine, 26, 507. https://doi.org/10.3892/etm.2023.12206
MLA
Tang, Z., Wang, Y., Liu, Y., Li, C."Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway". Experimental and Therapeutic Medicine 26.5 (2023): 507.
Chicago
Tang, Z., Wang, Y., Liu, Y., Li, C."Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway". Experimental and Therapeutic Medicine 26, no. 5 (2023): 507. https://doi.org/10.3892/etm.2023.12206
Copy and paste a formatted citation
x
Spandidos Publications style
Tang Z, Wang Y, Liu Y and Li C: Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway. Exp Ther Med 26: 507, 2023.
APA
Tang, Z., Wang, Y., Liu, Y., & Li, C. (2023). Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway. Experimental and Therapeutic Medicine, 26, 507. https://doi.org/10.3892/etm.2023.12206
MLA
Tang, Z., Wang, Y., Liu, Y., Li, C."Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway". Experimental and Therapeutic Medicine 26.5 (2023): 507.
Chicago
Tang, Z., Wang, Y., Liu, Y., Li, C."Salidroside inhibits renal ischemia/reperfusion injury‑induced ferroptosis by the PI3K/AKT signaling pathway". Experimental and Therapeutic Medicine 26, no. 5 (2023): 507. https://doi.org/10.3892/etm.2023.12206
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