Hosoi Toru, Suyama Yuka, Kayano Takaaki, Ozawa Koichiro
Department of Pharmacotherapy, Graduate School of Biomedical and Health Sciences, Hiroshima University Hiroshima, Japan.
Front Pharmacol. 2016 Sep 30;7:354. doi: 10.3389/fphar.2016.00354. eCollection 2016.
Leptin resistance is one of the mechanisms involved in the pathophysiology of obesity. The present study showed that glucose deprivation inhibited leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) and signal transducer and activator of transcription 5 (STAT5) in neuronal cells. Flurbiprofen reversed glucose deprivation-mediated attenuation of STAT3, but not STAT5 activation, in leptin-treated cells. Glucose deprivation increased C/EBP-homologous protein and glucose regulated protein 78 induction, indicating the activation of unfolded protein responses (UPR). Flurbiprofen did not affect the glucose deprivation-induced activation of UPR, but did attenuate the glucose deprivation-mediated induction of AMP-activated protein kinase phosphorylation. Flurbiprofen may ameliorate glucose deprivation-induced leptin resistance in neuronal cells.
瘦素抵抗是肥胖病理生理学涉及的机制之一。本研究表明，葡萄糖剥夺抑制了神经元细胞中瘦素诱导的信号转导和转录激活因子3（STAT3）及信号转导和转录激活因子5（STAT5）的磷酸化。氟比洛芬逆转了葡萄糖剥夺介导的瘦素处理细胞中STAT3的激活减弱，但未逆转STAT5的激活减弱。葡萄糖剥夺增加了C/EBP同源蛋白和葡萄糖调节蛋白78的诱导，表明未折叠蛋白反应（UPR）被激活。氟比洛芬不影响葡萄糖剥夺诱导的UPR激活，但确实减弱了葡萄糖剥夺介导的AMP激活蛋白激酶磷酸化的诱导。氟比洛芬可能改善神经元细胞中葡萄糖剥夺诱导的瘦素抵抗。
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