背景:莱菔硫烷可用于氧化应激相关疾病的治疗,血红素氧合酶是一种催化血红素降解的应激蛋白,已经成为预防氧化攻击的首选研究靶标之一.目的:观察核因子E2相关因子2激动剂莱菔硫烷对大鼠胰岛细胞系INS-1细胞血红素氧合酶1蛋白表达作用及细胞保护机制.方法:体外培养INS-1细胞,先用3 μmol/L莱菔硫烷进行干预培养3 h,再分别加入不同的胰岛素抵抗诱导剂葡萄糖氧化酶、地塞米松和葡萄糖胺刺激建立胰岛素抵抗细胞模型.结果与结论:3 μmol/L莱菔硫烷处理INS-1细胞中血红素氧合酶1的表达增加(P < 0.05),其效应在4 h后达到高峰(P < 0.05).3 μmol/L莱菔硫烷的预处理可逆转由胰岛素抵抗诱导剂导致的血红素氧合酶1表达下调(P < 0.05).而且在葡萄糖胺处理的INS-1细胞中,莱菔硫烷对血红素氧合酶1的表达改善与磷酸化PKB的表达上调具有正相关性(P < 0.05,r = 0.23).结果证实,莱菔硫烷可能通过诱导核因子E2相关因子2介导的血红素氧合酶1表达,增强胰岛细胞抗氧化防御功能和抗损伤信号系统,从而达到拮抗胰岛素抵抗诱导剂对胰岛细胞的损伤作用.%BACKGROUND: Sulforaphane (SFN) can be used for oxidative stress related disease's treatment. Heme oxygenas1 (HO-1) is a kind of enzyme degrading stress hemoglobin protein and HO-1 has become the first choice of anti-oxidation process. OBJECTIVE: To study the effect of SFN induced expression of HO-1 in a rat pancreatic beta cell line INS-1 and the potential cytoprotective mechanism of nuclear factor erythroid-related factor 2 (Nrf2). METHODS: During the culture of INS-1 cells, 3 μmol/L SFN was incubated for 3 hours and then glucose oxidase, dexamethasone and glucosamine were added to establish insulin resistance models. RESULTS AND CONCLUSION: The expression of HO-1 protein in INS-1 cells was increased after SFN (3μM) exposure, and reached the highest level after 4 hours exposure (P < 0.05). Decreased expression of HO-1 protein which was induced by inducers of insulin resistance could be reversed by SFN (3 μM) (P < 1 005). A positive correlation was found between the expression of HO-1 protein improved by SFN and the improved expression of protein kinase B phosphorylation in INS-1 cells treated with glucosamine (P < 0.05, r=0.23). SFN may enhance antioxidative defense in pancreatic beta cells through the induction of HO-1 via Nrf2 mediated transcription and enhance insulin signaling to protect beta cells from damaging.
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