相关实验视频

Updated: May 7, 2026

Invasion of Human Cells by a Bacterial Pathogen

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

欧戈斯特通过调节自和亡来保护犬类MDCK细胞免受胺素诱导的损伤

Zhipeng Qin¹, Liuwei Xie¹, Yao Wang¹

¹School of Police Dog Technology, Criminal Investigation Police University of China, Shenyang 110035, China.

|June 25, 2025

概括

埃尔戈斯特 (Erg) 通过减少氧化应激和炎症来保护狗细胞免受 gentamicin (GM) 诱导的损伤. 这种天然化合物通过恢复细胞活力和调节自和亡途径,显示出治疗犬损伤的潜力.

科学领域:

兽医医学兽医医学兽医医学
毒理学毒理学毒理学
细胞生物学细胞生物学

背景情况:

损伤是狗的重大健康问题,常常由诸如 gentamicin (GM) 等毒药物恶化.
甘胺素诱导的毒性会损害细胞,导致功能受损.
识别保护剂对于管理犬类药物诱导的脏损伤至关重要.

研究的目的:

调查埃尔戈斯特 (Erg) 对马丁-达比犬 (MDCK) 细胞中 gentamicin (GM) 诱导的毒性的保护作用.
阐明Erg保护作用的基本机制,包括其对氧化应激,炎症,自和亡的影响.
评估Ergosterol作为治疗犬损伤的治疗剂的潜力.

主要方法:

MDCK细胞暴露在 gentamicin (GM) 中以诱导毒性.
在暴露于转基因生物之前,对欧戈斯特 (Erg) 进行了预处理,以评估其保护作用.
评估了细胞活力,氧化 (NO),乳酸脱酶 (LDH),氧化应激标志物 (SOD,GSH,CAT,MDA),炎症细胞因子 (IL-1β,IL-6,TNF-α),功能指标 (Scr,BUN) 和与自/亡相关的蛋白质.
测试包括CCK-8,ELISA,光染色和西方斑点分析.

主要成果:

甘胺显著降低了细胞活力,增加了NO和LDH水平,表明细胞受损.
埃尔戈斯特前处理恢复了细胞活力,抑制了NO和LDH的释放,并增强了抗氧化酶的活性.
埃尔戈斯特减弱了转基因诱导的活性氧物种 (ROS) 的过度产量,并降低了促炎性细胞因子.
欧戈斯特上调自蛋白 (ATG5,Beclin1),减少P62积累,并降低BAX/BCL-2比率,表明自和亡的调节.

结论:

埃尔戈斯特 (Erg) 在狗细胞中显示出显著的保护作用,防止 gentamicin (GM) 诱导的毒性.
埃尔格的机制包括恢复自流,抑制线粒体亡,减轻氧化应激和炎症.
这些发现表明埃尔戈斯特作为狗损伤的天然治疗剂的潜力,需要进一步的体内调查.

关键词:

的细胞MDCK细胞.灭症 (apoptosis) 是一种死亡的过程.自自是自的过程.埃尔戈斯醇 (Ergosterol) 是一种这是一种 gentamicin 药物.氧化应激是一种氧化应激.保护脏保护脏

更多相关视频

Dissection of Adult Mouse Utricle and Adenovirus-mediated Supporting-cell Infection

Dissection of Adult Mouse Utricle and Adenovirus-mediated Supporting-cell Infection

Published on: March 28, 2012

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

相关概念视频

Autophagic Cell Death

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

Antifungal Agents

Antifungal Agents

Amphotericin B is a broad-spectrum antifungal agent that exploits structural differences between fungal and mammalian cell membranes. Its amphipathic structure—featuring a hydrophobic polyene-lactone ring and a hydrophilic region containing mycosamine and carboxylic acid groups—enables selective binding to ergosterol, a sterol predominantly found in fungal plasma membranes. This selective interaction underlies the drug’s antifungal activity, although weak binding to cholesterol contributes to...

Cellular Injury V: Apoptosis and Autophagy

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...