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减少NrF2作为辅助剂,在持续的周周病变的发展过程中

C Guerrero-Bobadilla¹, I Yáñez-Sánchez, T Franco-Ávila

¹Department of Microbiology and Pathology CUCS, University of Guadalajara Sierra Mojada 950, Col. Centro C.P. 44340, Guadalajara, Jalisco, México galvez1975@gmail.com.

Medicina oral, patologia oral y cirugia bucal

|June 18, 2023

概括

持续的周周病变 (PPL) 与氧化应激和降低抗氧化防御有关. 这项研究发现,减少Nrf2控制的抗氧化剂与PPL患者的骨损伤相关.

科学领域:

牙周内科医院牙周内科医院牙周内科医院
口腔病理学口腔病理学
生物化学生物化学

背景情况:

持续的周周病变 (PPL) 是由细菌感染引起的,导致脉死亡,骨质退化和牙脱落.
周围组织的病理变化与自由基的存在和氧化应激有关.
核因子红色素2相关因子2 (Nrf2) 调节内源性抗氧化反应和骨质细胞生成.

研究的目的:

为了研究持久的周周病变样本中的氧化状态.
为了确定氧化应激是否作为围组织损伤的一个因素.

主要方法:

观察性,描述性,横截面研究,比较PPL样本 (病例) 与第三移除样本 (对照).
使用血素-氨酸染色的组织学分析.
生物化学测定脂质过氧化,超氧化解化酶 (SOD),氨酸氧化酶 (GPx) 和催化酶 (CAT) 活动.
西部布洛特对Nrf2蛋白水平的分析.

主要成果:

PPL样本显示了淋巴细胞,血细胞和埃索诺菲尔细胞的增加,细胞外矩阵蛋白和纤维细胞的减少.
在PPL样本中观察到升高的脂质过氧化,GPx和SOD活动.
与对照组相比,在PPL病例中发现了catalase活性 (36%) 和nrf2蛋白 (10.41%) 的显著下降.

结论:

控制Nrf2的内源性抗氧化剂的变化与PPL患者的骨质破坏有关.
氧化应激似乎在持续的周周病变的发病过程中发挥着重要作用.

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