Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling

  • Authors:
    • Shao Zhong
    • Jing Ge
    • Jiang‑Yi Yu
  • View Affiliations

  • Published online on: July 20, 2018     https://doi.org/10.3892/etm.2018.6502
  • Pages: 2756-2762
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Abstract

The loss of insulin secretion in type I diabetes mellitus (T1DM) is caused by autoimmune‑mediated destruction of insulin‑producing pancreatic β‑cells. Inflammatory cytokines and immune cell infiltration activate oxidative and endoplasmic reticulum (ER) stress, resulting in reduced β‑cell viability. The current pharmacological agents used to control blood glucose have a limited effective duration and are accompanied by strong side effects. Blocking the inflammatory and immune responses that cause the β‑cell damage has been investigated as a novel therapeutic approach to control T1DM. Icariin is a flavonoid component of Chinese medicinal herbs that has anti‑inflammatory effects in vitro and in vivo. The results of the present study revealed that icariin abrogates the pro‑apoptotic effect of inflammatory cytokines and significantly suppresses the activation of nuclear factor (NF)‑κB in rat pancreatic β‑cell lines. The present study may provide a basis for the potential use of icariin as a therapeutic agent for T1DM.
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September-2018
Volume 16 Issue 3

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

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Spandidos Publications style
Zhong S, Ge J and Yu JY: Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling. Exp Ther Med 16: 2756-2762, 2018.
APA
Zhong, S., Ge, J., & Yu, J. (2018). Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling. Experimental and Therapeutic Medicine, 16, 2756-2762. https://doi.org/10.3892/etm.2018.6502
MLA
Zhong, S., Ge, J., Yu, J."Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling". Experimental and Therapeutic Medicine 16.3 (2018): 2756-2762.
Chicago
Zhong, S., Ge, J., Yu, J."Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling". Experimental and Therapeutic Medicine 16, no. 3 (2018): 2756-2762. https://doi.org/10.3892/etm.2018.6502