关键词: apoptosis deoxynivalenol glucose absorption capacity inflammatory injury porcine small intestinal epithelial cells

Mesh : Animals Trichothecenes / toxicity Swine Glucose / metabolism Epithelial Cells / drug effects metabolism Sodium-Glucose Transporter 1 / metabolism genetics Cell Line Intestine, Small / drug effects Inflammation / chemically induced Cytokines / metabolism genetics Biological Transport / drug effects Glucose Transporter Type 2 / metabolism genetics Apoptosis / drug effects Intestinal Mucosa / drug effects metabolism

来  源:   DOI:10.1093/jas/skae107   PDF(Pubmed)

Abstract:
The present study aimed to investigate the effects of deoxynivalenol (DON) stimulation on inflammatory injury and the expression of the glucose transporters sodium-dependent glucose transporter 1 (SGLT1) and glucose transporter protein 2 (GLU2) in porcine small intestinal epithelial cells (IPEC-J2). Additionally, the study aimed to provide initial insights into the connection between the expression of glucose transporters and the inflammatory injury of IPEC-J2 cells. DON concentration and DON treatment time were determined using the CCK‑8 assay. Accordingly, 1.0 µg/mL DON and treatment for 24 h were chosen for subsequent experiments. Then IPEC-J2 cells were treated without DON (CON, N = 6) or with 1 μg/mL DON (DON, N = 6). Lactate dehydrogenase (LDH) content, apoptosis rate, and proinflammatory cytokines including interleukin (IL)-1β, Il-6, and tumor necrosis factor α (TNF-α) were measured. Additionally, the expression of AMP-activated protein kinase α1 (AMPK-α1), the content of glucose, intestinal alkaline phosphatase (AKP), and sodium/potassium-transporting adenosine triphosphatase (Na+/K+-ATPase) activity, and the expression of SGLT1 and GLU2 of IPEC-J2 cells were also analyzed. The results showed that DON exposure significantly increased LDH release and apoptosis rate of IPEC-J2 cells. Stimulation with DON resulted in significant cellular inflammatory damage, as evidenced by a significant increase in proinflammatory cytokines (IL-1β, IL-6, and TNF-α). Additionally, DON caused damage to the glucose absorption capacity of IPEC-J2 cells, indicated by decreased levels of glucose content, AKP activity, Na+/K+-ATPase activity, AMPK-α1 protein expression, and SGLT1 expression. Correlation analysis revealed that glucose absorption capacity was negatively correlated with cell inflammatory cytokines. Based on the findings of this study, it can be preliminarily concluded that the cell inflammatory damage caused by DON may be associated with decreased glucose absorption.
Glucose is one of the most basic nutrients necessary to sustain animal life and plays a crucial role in animal body composition and energy metabolism. Previous studies suggested a link between glucose absorption and inflammatory injury. In the present study, deoxynivalenol (DON) stimulation caused severe inflammatory injury and reduced the glucose absorption capacity of IPEC-J2 cells. Pearson’s correlation analysis revealed a negative correlation between glucose absorption capacity and cell inflammatory cytokines. Ultimately, it can be speculated that the cellular inflammatory response triggered by DON may be related to the altered expression of glucose transporters.
摘要:
本研究旨在探讨脱氧雪腐镰刀菌烯醇(DON)刺激对猪小肠上皮细胞(IPEC-J2)炎症损伤及葡萄糖转运蛋白钠依赖性葡萄糖转运蛋白1(SGLT1)和葡萄糖转运蛋白2(GLU2)表达的影响。此外,本研究旨在对葡萄糖转运蛋白的表达与IPEC-J2细胞的炎症损伤之间的联系提供初步的见解。使用CCK‑8测定法测定DON浓度和DON处理时间。因此,选择1.0μg/mLDON并处理24小时用于后续实验。然后用无DON处理IPEC-J2细胞(CON,N=6)或1μg/mLDON(DON,N=6)。乳酸脱氢酶(LDH)含量,凋亡率,和促炎细胞因子,包括白细胞介素(IL)-1β,测量IL-6和肿瘤坏死因子α(TNF-α)。此外,AMP激活蛋白激酶α1(AMPK-α1)的表达,葡萄糖的含量,肠碱性磷酸酶(AKP)和钠/钾转运腺苷三磷酸酶(Na/K-ATPase)活性,同时分析了IPEC-J2细胞中SGLT1和GLU2的表达。结果表明,DON暴露显著增加IPEC-J2细胞的LDH释放和凋亡率。用DON刺激导致显著的细胞炎症损伤,正如促炎细胞因子(IL-1β,IL-6和TNF-α)。此外,DON对IPEC-J2细胞的葡萄糖吸收能力造成损害,葡萄糖含量水平下降,AKP活动,Na+/K+-ATP酶活性,AMPK-α1蛋白表达,和SGLT1表达式。相关分析表明,葡萄糖吸收能力与细胞炎性细胞因子呈负相关。根据这项研究的结果,由此可以初步得出结论,DON引起的细胞炎症损伤可能与葡萄糖吸收减少有关。
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