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Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling

  • Authors:
    • Lulu Ji
    • Qing She
    • Ping Zhou
    • Yibin Qin
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China
    Copyright: © Ji et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 8
    |
    Published online on: November 10, 2023
       https://doi.org/10.3892/etm.2023.12295
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Abstract

Butorphanol is a synthetic selective opioid receptor antagonist that exhibits substantial analgesic effects. The present study aimed to explore the effects of butorphanol on a neurodegenerative disease cell model and to investigate its specific regulatory mechanism. Cell viability of PC12 cells was assessed using the Cell Counting Kit‑8 assay. Oxidative stress levels were measured by the corresponding kits and western blotting of specific protein markers. Apoptosis was determined using the terminal‑deoxynucleoitidyl transferase mediated nick end labeling assay and by western blotting. Western blotting was used to analyze the expression levels of c‑Jun NH2‑terminal kinase (JNK)/p38 signaling pathway‑related proteins. Thiobarbituric acid‑reactive substances and Fe+2 content were detected using the corresponding assay kits and the expression levels of ferroptosis‑associated proteins were assessed by western blotting following the addition of the JNK activator anisomycin (ANI). Oxidative stress and apoptosis were examined with the aforementioned assays following the supplementation of ANI or the ferroptosis inducer erastin (ERA). It was revealed that butorphanol dose‑dependently enhanced the viability and suppressed the oxidative stress and apoptosis of H2O2‑treated PC12 cells. In addition, butorphanol blocked JNK/p38 signaling and hampered ferroptosis, while this effect was reversed by ANI. ANI or ERA reversed the effects of butorphanol on oxidative stress and apoptosis of H2O2‑treated PC12 cells. In summary, butorphanol suppressed ferroptosis by blocking JNK/p38 signaling to impart inhibitory effects on oxidative stress and apoptosis in a neurodegenerative disease cell model.
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Copy and paste a formatted citation
Spandidos Publications style
Ji L, She Q, Zhou P and Qin Y: Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling. Exp Ther Med 27: 8, 2024.
APA
Ji, L., She, Q., Zhou, P., & Qin, Y. (2024). Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling. Experimental and Therapeutic Medicine, 27, 8. https://doi.org/10.3892/etm.2023.12295
MLA
Ji, L., She, Q., Zhou, P., Qin, Y."Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling". Experimental and Therapeutic Medicine 27.1 (2024): 8.
Chicago
Ji, L., She, Q., Zhou, P., Qin, Y."Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling". Experimental and Therapeutic Medicine 27, no. 1 (2024): 8. https://doi.org/10.3892/etm.2023.12295
Copy and paste a formatted citation
x
Spandidos Publications style
Ji L, She Q, Zhou P and Qin Y: Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling. Exp Ther Med 27: 8, 2024.
APA
Ji, L., She, Q., Zhou, P., & Qin, Y. (2024). Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling. Experimental and Therapeutic Medicine, 27, 8. https://doi.org/10.3892/etm.2023.12295
MLA
Ji, L., She, Q., Zhou, P., Qin, Y."Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling". Experimental and Therapeutic Medicine 27.1 (2024): 8.
Chicago
Ji, L., She, Q., Zhou, P., Qin, Y."Butorphanol inhibits ferroptosis to attenuate PC12 cell injury by blocking JNK/p38 signaling". Experimental and Therapeutic Medicine 27, no. 1 (2024): 8. https://doi.org/10.3892/etm.2023.12295
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