暴露于会通过抑制糖尿病大鼠的自来加剧损伤
Yonggang Ma1, Chenguang Yue1, Qiannan Sun2
1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu 225009, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu 225009, PR China; Joint International Research Laboratory of Agriculture and Agri-Product Safety of the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu 225009, PR China.
Ecotoxicology and environmental safety
|November 12, 2023
概括
暴露会通过抑制自而使糖尿病损伤恶化. 这项针对糖尿病大鼠和细胞的研究揭示了的含量.
科学领域:
- 毒理学和环境健康
- 科和脏疾病.
- 细胞生物学和自
背景情况:
- 糖尿病 (DM) 发病率在全球范围内不断上升,这对健康构成了重大挑战.
- (Cd) 是一种普遍存在的环境毒素,被怀疑会导致糖尿病病 (DN).
- 关联暴露与DN病变的确切机制在很大程度上仍未确定.
研究的目的:
- 调查暴露对糖尿病大鼠损伤的有害影响.
- 阐明基底的分子机制,特别是专注于自,在诱导的DN.
- 在糖尿病的背景下,为的毒性通路提供新的见解.
主要方法:
- 组织病理学分析 (HE,PAS,马森染色) 的脏组织.
- 免疫组织化学和西式斑点测试用于量化蛋白质水平 (COL-I,COL-IV,CTSB,CTSD,p62,LC3).
- 传输电子显微镜 (TEM) 评估线粒体超结构和自细胞形成.
- 对氧化应激标志物 (MDA,GSH,CAT,SOD,GSH-PX) 和尿液/血清肌素的生物化学测定.
主要成果:
- 在糖尿病大鼠中,暴露加剧了损伤,增加了尿路微专/肌素,并减少了肌素清除.
- 氧化应激标志物发生显著变化,MDA增加和暴露后抗氧化酶活性降低.
- 暴露抑制了自 (降低p62/LC3比率,降低 lysosomal 蛋白质) 和增加亡和纤维化在细胞和组织.
结论:
- 在动物模型和管细胞中,暴露显著加剧了糖尿病损伤.
- 糖尿病中的毒性在一定程度上是通过抑制自途径来调节的.
- 这些发现强调了自作为理解和潜在地减轻糖尿病患者中诱导的损伤的关键目标.
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