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Glucose Starvation-Caused Oxidative Stress Induces Inflammation and Autophagy in Human Gingival Fibroblasts
Antioxidants ( IF 7 ) Pub Date : 2022-09-26 , DOI: 10.3390/antiox11101907
Runbo Li 1 , Hirohito Kato 1 , Yoichiro Taguchi 1 , Xin Deng 1 , Emika Minagawa 1 , Takaya Nakata 1 , Makoto Umeda 1
Affiliation  

Gingival tissue experiences an environment of nutrient shortage, such as low glucose conditions, after periodontal surgery. Our previous studies found that this low glucose condition inhibits normal gingival cell functions. However, the mechanism by which this glucose-deficient environment causes cellular damage to human gingival fibroblasts (HGnFs) remains unclear. This study aimed to investigate the biological effects of ROS induction on HGnFs under low glucose conditions. ROS levels and cellular anti-ROS ability of HGnFs under different glucose concentrations were evaluated by measuring ROS formation and the expression of superoxide dismutase and heme oxygenase 1. Changes in cellular viability were investigated using 5-bromo-2′-deoxyuridine assay and cell survival detection, and the cellular damage was evaluated by the expression of inflammatory cytokines and changes in the expression of autophagy-related protein. ROS formation was then blocked using N-acetyl-L-cysteine (NAC), and the effects of ROS on HGnFs under low glucose conditions were investigated. Low glucose conditions induced ROS accumulation, reduced cellular activity, and induced inflammation and autophagy. After NAC application, the anti-ROS capacity increased, cellular activity improved, and inflammation and autophagy were controlled. This can be effectively controlled by the application of antioxidants such as NAC.

中文翻译:

葡萄糖饥饿引起的氧化应激诱导人牙龈成纤维细胞的炎症和自噬

牙周手术后,牙龈组织经历了营养缺乏的环境,例如低葡萄糖条件。我们之前的研究发现,这种低血糖状态会抑制正常的牙龈细胞功能。然而,这种葡萄糖缺乏环境对人牙龈成纤维细胞 (HGnF) 造成细胞损伤的机制仍不清楚。本研究旨在研究低葡萄糖条件下 ROS 诱导对 HGnFs 的生物学效应。通过测量 ROS 形成以及超氧化物歧化酶和血红素加氧酶 1 的表达来评估 HGnF 在不同葡萄糖浓度下的 ROS 水平和细胞抗 ROS 能力。使用 5-bromo-2'-deoxyuridine 测定和细胞存活率研究细胞活力的变化检测,并通过炎性细胞因子的表达和自噬相关蛋白表达的变化来评估细胞损伤。然后使用 N-乙酰基-L-半胱氨酸 (NAC) 阻断 ROS 的形成,并研究了 ROS 在低葡萄糖条件下对 HGnFs 的影响。低葡萄糖条件诱导 ROS 积累,降低细胞活性,并诱导炎症和自噬。NAC应用后,抗ROS能力增加,细胞活性提高,炎症和自噬得到控制。这可以通过使用抗氧化剂如 NAC 来有效控制。低葡萄糖条件诱导 ROS 积累,降低细胞活性,并诱导炎症和自噬。NAC应用后,抗ROS能力增加,细胞活性提高,炎症和自噬得到控制。这可以通过使用抗氧化剂如 NAC 来有效控制。低葡萄糖条件诱导 ROS 积累,降低细胞活性,并诱导炎症和自噬。NAC应用后,抗ROS能力增加,细胞活性提高,炎症和自噬得到控制。这可以通过使用抗氧化剂如 NAC 来有效控制。
更新日期:2022-09-26
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