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Formononetin Attenuates IL-1β-Induced Apoptosis and NF-κB Activation in INS-1 Cells

By Xiao Han, Zhengqiu Zhu, Dong Wang, Zuoling Xie, Han Yin, Yunxia Zhu, Lu Gao and Yao Wang

Abstract

Several studies suggest that the inflammation plays a role in the pathogenesis of some glucose disorders in adults. Exposure of pancreatic β-cells to cytokines, such as interleukin-1β (IL-1β), is thought to contribute to β-cell apoptosis. One important event triggered by IL-1β is induction of nitric oxide synthase (iNOS), an enzyme that catalyzes intracellular generation of the cytotoxic free radical NO. Recent work have suggested that formononetin, as an <em>O</em>-methylated isoflavone found in a number of plants and herbs like <em>Astragalus membranaceus</em>, inhibited some pro-inflammatory cytokine production in macrophages. However, the roles of formononetin in pancreatic beta cells have not been fully established. The aim of the present study was to assess possible <em>in vitro</em> effects of formononetin on cell apoptosis induced by IL-1β in the rat insulinoma cell line, INS-1. Our results demonstrate that formononetin significantly prevents IL-1β-increased INS-1 cell death and blocks cytokine-induced apoptotic signaling (the reduction of Bax/Bcl-2 ratio and caspase-3 activity). Formononetin also inhibited the activation of nuclear factor-kappaB (NF-κB), which is a significant transcription factor for iNOS, so as to decease nitric oxide (NO) formation in a dose dependent manner <em>in vitro</em>. Our observations indicated that formononetin could protect against pancreatic β-cell apoptosis caused by IL-1β and therefore could be used in the future as a new drug improving diabetes mellitus

Topics: <em>INS-1</em>, NF-κB, iNOS, formononetin, apoptosis, Organic chemistry, QD241-441, Chemistry, QD1-999, Science, Q, DOAJ:Organic Chemistry, DOAJ:Chemistry
Publisher: MDPI AG
Year: 2012
DOI identifier: 10.3390/molecules170910052
OAI identifier: oai:doaj.org/article:0b5f96a31f474952808c596a6202aead
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