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高流动性组第1框 (HMGB1) 中介尼古丁诱导的细胞损伤

Sayantap Datta¹, Mohammad Atiqur Rahman¹, Saisudha Koka²

¹Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, United States.

Frontiers in pharmacology

|January 22, 2025

概括

高流动性组第1框 (HMGB1) 中介尼古丁诱导的细胞损伤. 甘油抑制了HMGB1的释放和受保护的皮细胞功能,突出了HMGB1的功能.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
毒理学毒理学毒理学

背景情况:

吸烟是功能障碍的一个已知的危险因素.
连接吸烟与损伤的分子机制尚未完全理解.
高流动性组框1 (HMGB1) 涉及炎症和自身免疫性疾病,包括慢性病.

研究的目的:

调查HMGB1在尼古丁诱导的细胞损伤中的作用.
探索甘油 (Gly) 对尼古丁诱导的 podocyte 损伤的潜在保护作用.

主要方法:

细胞被用尼古丁和/或草甘治疗.
测量了HMGB1的表达和释放.
评估了细胞标记物 (podocin,nephrin) 和损伤标记物 (desmin) 的表达.
评估了细胞的透性.
分析了托尔类受体4 (TLR4) 的表达和激活.

主要成果:

尼古丁增加了HMGB1的表达和释放.
草甘治疗降低了HMGB1水平,并保护了细胞功能蛋白 (podocin,nephrin).
尼古丁增加了desmin表达和细胞透性,而Gly.减弱了这些作用.
尼古丁上调TLR4表达,而这被Gly和TLR4抑制剂 (Resatorvid) 抑制.

结论:

HMGB1是尼古丁诱导的细胞损伤的关键调解者.
HMGB1至少部分通过激活TLR4.1来发挥其作用.
甘油显示出作为治疗剂的潜力,通过抑制HMGB1和保护 podocytes.

关键词:

这就是HMGB1的特点.在TLR4中,尼古丁是一种尼古丁.葡萄细胞 (podocytes) 是一个细胞.吸烟是为了吸烟.

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