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

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.