ABSTRACT β-Conglycinin and glycinin are known to induce various allergic reactions, however, but little is known about the mechanism underlying the development of allergy to soybean antigen proteins. In this study, porcine intestinal epithelial cells (IPEC-J2) were used to investigate the effects of soybean antigen proteins, β-conglycinin and glycinin, on cells to determine whether the caspase-3/mitochondrion-regulated apoptotic pathway underlies the allergic reaction. IPEC-J2 cells were treated with different concentrations (0, 5, and 10 mg mL−1) of β-conglycinin or glycinin, and 50 μM z-DEVD-FMK (a caspase-3 inhibitor). The results show that the apoptosis rate, mitochondrion-regulated mRNA and protein expression levels, caspase-3 activation, cyt-c release, cytoskeleton and tight junction protein expression, mitochondrial membrane potential depolarization and mitochondrial injury were significantly aggravated with cultured in increasing concentrations of β-conglycinin or glycinin. While these effects were inhibited by application of the caspase-3 inhibitor. Thus, we concluded that β-conglycinin and glycinin cause IPEC-J2 cell apoptosis via the caspase-3/mitochondrion-regulated apoptotic pathway.

中文翻译：

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大豆抗原蛋白诱导 IPEC-J2 细胞中 caspase-3/线粒体调节的细胞凋亡

摘要 β-伴大豆球蛋白和大豆球蛋白已知会诱发各种过敏反应，但对大豆抗原蛋白过敏发展的潜在机制知之甚少。在本研究中，猪肠上皮细胞 (IPEC-J2) 用于研究大豆抗原蛋白、β-伴大豆球蛋白和大豆球蛋白对细胞的影响，以确定 caspase-3/线粒体调节的凋亡途径是否是过敏反应的基础。IPEC-J2 细胞用不同浓度（0、5 和 10 mg mL-1）的 β-伴大豆球蛋白或大豆球蛋白以及 50 μM z-DEVD-FMK（一种 caspase-3 抑制剂）处理。结果表明，细胞凋亡率、线粒体调控的 mRNA 和蛋白表达水平、caspase-3 激活、cyt-c 释放、细胞骨架和紧密连接蛋白表达、随着β-伴大豆球蛋白或大豆球蛋白浓度的增加，线粒体膜电位去极化和线粒体损伤显着加重。虽然这些作用被 caspase-3 抑制剂的应用所抑制。因此，我们得出结论，β-伴大豆球蛋白和大豆球蛋白通过 caspase-3/线粒体调节的凋亡途径引起 IPEC-J2 细胞凋亡。