首页> 外文会议>Annual Meeting of the Japanese Association for Animal Cell Technology >ANALYSIS OF THE MECHANISM OF THE TIGHT-JUNCTIONAL PERMEABILITY INCREASE BY CAPSAICIN TREATMENT ON THE INTESTINAL CACO-2 CELL
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ANALYSIS OF THE MECHANISM OF THE TIGHT-JUNCTIONAL PERMEABILITY INCREASE BY CAPSAICIN TREATMENT ON THE INTESTINAL CACO-2 CELL

机译:辣椒素处理对肠道Caco-2细胞的辣椒素治疗的紧张渗透性机理分析

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In a previous experiment (Isoda et al., 2001), we showed that the tight-junctional (TJ) permeability increase in Caco-2 cells during capsaicin exposure was through binding of the capsaicin molecule to a capsaicin receptor-like protein. In the presentstudy, we examined how actin, which modulates TJ permeability, is influenced by capsaicin. We showed that after treatment of the Caco-2 cells with capsaicin, the volume of F-actin decreased. Moreover, we also examined protein kinase C (PKC) and heat shock protein 47 (HSP47), which act as probable second messengers in causing TJ permeability increase. We showed that after capsaicin treatment, HSP47 was activated. However, PKC activity was the same in both control and treatment setups. These results suggest that, while PKC is not involved, it is highly possible that HSP47 plays a role in TJ permeability increase in intestinal Caco-2 cells exposed to capsaicin.
机译:在先前的实验中(Isoda等,2001),我们表明,在辣椒素暴露期间CaCo-2细胞的紧密连接(TJ)渗透性是通过辣椒素分子与辣椒素受体样蛋白质的结合。在术语中,我们检查了如何调节TJ渗透性的肌动蛋白是受辣椒素的影响。我们表明,在用辣椒素处理CaCO-2细胞后,F-Actin的体积减少。此外,我们还检查了蛋白激酶C(PKC)和热休克蛋白47(HSP47),其充当可能的第二信使导致TJ渗透率增加。我们表明,在辣椒素治疗后,HSP47被激活。然而,在控制和治疗设置中,PKC活性是相同的。这些结果表明,虽然不涉及PKC,但HSP47非常可能在暴露于辣椒素的肠道Caco-2细胞中的TJ渗透性增加中发挥作用。

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