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The cytoprotective role of omentin against oxidative stress-induced PC12 apoptosis

机译:甲壳素对氧化应激诱导的PC12细胞凋亡的细胞保护作用

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Oxidative stress has been proven to play a critical role in the pathogenesis of neuronal injury. As a novel adipocytokine, omentin is produced by visceral adipose with insulin sensitizing effects and has been revealed to possess anti-inflammatory effects. However, the possible effect of omentin on oxidative stress remains unknown. The present study aimed to detect the potential protective effect of omentin against hydrogen peroxide (H 2 O 2 )-induced cytotoxicity of PC12 cells. The results showed that no cytotoxic effect was shown in PC12 cells co-cultured with omentin alone at a concentration of 50–1000?ng/mL. The CCK8 and TUNEL assays suggested that omentin could remarkably attenuate apoptosis induced by 100?μM H 2 O 2 . The PCR and western blotting showed that the expression levels of Bax was significantly inhibited by omentin via the upregulation of miR-128-3p at its 3′-UTR. Taken together, these results indicated that omentin protects PC12 cells against H 2 O 2 -induced apoptosis, and further studies need to be conducted before utilization in the clinic for the treatment of neurodegenerative diseases.
机译:已被证明氧化应激在神经元损伤的发病机制中发挥着关键作用。作为一种新型脂肪蛋白,Omentin由具有胰岛素敏化作用的内脏脂肪产生,并且已经显示出具有抗炎作用。然而,甲壳素在氧化应激上的可能影响仍然是未知的。本研究旨在检测甲壳素对过氧化氢(H 2 O 2)的潜在保护作用 - 诱导PC12细胞的细胞毒性。结果表明,在浓度为50-1000×ng / ml的浓度下,在PC12细胞中没有显示细胞毒性效应。 CCK8和TUNEL测定表明,本心素可以显着衰减100μmH2 O 2的凋亡。 PCR和Western印迹表明,通过在其3'-UTR下通过MiR-128-3P的上调,Opentin显着抑制了Bax的表达水平。总之,这些结果表明,本心素保护PC12细胞免受H 2 O 2-2 O 2诱导的细胞凋亡,并且需要进一步研究在使用前进行诊所治疗神经退行性疾病。

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