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5-Hydroxymethylfurfural Exerts Negative Effects on Gastric Mucosal Epithelial Cells by Inducing Oxidative Stress, Apoptosis, and Tight Junction Disruption
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2022-03-21 , DOI: 10.1021/acs.jafc.2c00269 Yanting Qiu 1 , Xiaorong Lin 1 , Zhongzheng Chen 1 , Bin Li 1 , Yuanyuan Zhang 1
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2022-03-21 , DOI: 10.1021/acs.jafc.2c00269 Yanting Qiu 1 , Xiaorong Lin 1 , Zhongzheng Chen 1 , Bin Li 1 , Yuanyuan Zhang 1
Affiliation
5-Hydroxymethylfurfural (5-HMF) is a processing byproduct present in foods that are consumed daily by humans, and the diet is the principal route for human exposure to it. However, its adverse effects on gastric epithelial cells are not fully understood. Based on the half inhibitory concentration value, concentrations of HMF of 2, 4, 8, and 16 mM were selected for this study. After 5-HMF treatment for 24 h, the number of living cells decreased to 89.61 ± 0.48, 77.30 ± 0.57, 58.75 ± 0.36, and 19.61 ± 0.40% of the control, respectively. Apoptosis activated through both the death receptor and mitochondrial pathways was confirmed to be the primary mode of HMF-induced cell death. Further analysis revealed that the reactive oxygen species (ROS) levels in GES-1 cells increased 1.7–6.5 fold after exposure to 5-HMF. Moreover, the inhibition of ROS by N-acetylcysteine blocked HMF-induced apoptosis and cell proliferation suppression, indicating that oxidative stress was important in HMF-induced apoptosis. Besides, after 5-HMF treatment, the gene expressions of occludin and ZO-1 were reduced by 1.1–3.4 fold and 2.0–9.4 fold, respectively. The cell surface morphology and tight junction-related protein expression analysis also revealed the destructive effect of 5-HMF on tight junction integrity. Our research highlights a potential mechanism of HMF-induced toxicity in GES-1 cells and provides additional information on the health risks of 5-HMF exposure to the human gastric epithelium.
中文翻译:
5-羟甲基糠醛通过诱导氧化应激、细胞凋亡和紧密连接破坏对胃粘膜上皮细胞产生负面影响
5-羟甲基糠醛 (5-HMF) 是人类日常食用的食物中存在的加工副产品,饮食是人类接触它的主要途径。然而,其对胃上皮细胞的不利影响尚不完全清楚。基于半抑制浓度值,本研究选择了 2、4、8 和 16 mM 的 HMF 浓度。5-HMF 处理 24 小时后,活细胞数量分别减少到对照组的 89.61 ± 0.48、77.30 ± 0.57、58.75 ± 0.36 和 19.61 ± 0.40%。通过死亡受体和线粒体途径激活的细胞凋亡被证实是 HMF 诱导的细胞死亡的主要模式。进一步分析表明,暴露于 5-HMF 后,GES-1 细胞中的活性氧 (ROS) 水平增加了 1.7-6.5 倍。此外,通过抑制 ROSN-乙酰半胱氨酸阻断HMF诱导的细胞凋亡和细胞增殖抑制,表明氧化应激在HMF诱导的细胞凋亡中很重要。此外,5-HMF处理后,occludin和ZO-1的基因表达分别降低了1.1-3.4倍和2.0-9.4倍。细胞表面形态和紧密连接相关蛋白表达分析也揭示了 5-HMF 对紧密连接完整性的破坏作用。我们的研究强调了 HMF 诱导 GES-1 细胞毒性的潜在机制,并提供了有关 5-HMF 暴露于人胃上皮细胞的健康风险的更多信息。
更新日期:2022-03-21
中文翻译:
5-羟甲基糠醛通过诱导氧化应激、细胞凋亡和紧密连接破坏对胃粘膜上皮细胞产生负面影响
5-羟甲基糠醛 (5-HMF) 是人类日常食用的食物中存在的加工副产品,饮食是人类接触它的主要途径。然而,其对胃上皮细胞的不利影响尚不完全清楚。基于半抑制浓度值,本研究选择了 2、4、8 和 16 mM 的 HMF 浓度。5-HMF 处理 24 小时后,活细胞数量分别减少到对照组的 89.61 ± 0.48、77.30 ± 0.57、58.75 ± 0.36 和 19.61 ± 0.40%。通过死亡受体和线粒体途径激活的细胞凋亡被证实是 HMF 诱导的细胞死亡的主要模式。进一步分析表明,暴露于 5-HMF 后,GES-1 细胞中的活性氧 (ROS) 水平增加了 1.7-6.5 倍。此外,通过抑制 ROSN-乙酰半胱氨酸阻断HMF诱导的细胞凋亡和细胞增殖抑制,表明氧化应激在HMF诱导的细胞凋亡中很重要。此外,5-HMF处理后,occludin和ZO-1的基因表达分别降低了1.1-3.4倍和2.0-9.4倍。细胞表面形态和紧密连接相关蛋白表达分析也揭示了 5-HMF 对紧密连接完整性的破坏作用。我们的研究强调了 HMF 诱导 GES-1 细胞毒性的潜在机制,并提供了有关 5-HMF 暴露于人胃上皮细胞的健康风险的更多信息。