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槲皮素对氯化钯诱导的肝肾组织内质网应激、炎症、氧化应激和细胞凋亡的影响

Effects of Quercetin on Palladium Chloride-Induced Endoplasmic Reticulum Stress, Inflammation, Oxidative Stress, and Apoptosis in Hepatorenal Tissues.

作者信息

Adiguzel Caglar, Karaboduk Hatice, Apaydın Fatma Gokce, Kalender Yusuf

机构信息

Department of Biology, Faculty of Science, Gazi University, 06500 Ankara, Türkiye.

出版信息

Microsc Microanal. 2025 Jul 15;31(4). doi: 10.1093/mam/ozaf077.

Abstract

To understand the potential hazards of palladium particles dispersed in the environment, comprehensive toxicological studies are required. Quercetin (Que) is a natural flavonoid compound with antioxidant properties. This study was conducted to investigate the potential protective effects of Que (30 mg/kg bw) usage against oxidative stress, apoptosis, inflammation, and endoplasmic reticulum (ER) stress damage in palladium chloride (PdCl2) (8 mg/kg bw)-induced hepatorenal toxicity in rats. As a result of 28 days of PdCl2 application, antioxidant capacity (SOD, CAT, GPx, and GST) in hepatorenal tissues decreased, and the MDA level, which is a marker of lipid peroxidation, increased. In addition, changes were determined in markers such as ALT, AST, LDH, urea, and creatinine in serum. Similarly, PON-1 and AChE activities decreased and NO, 8-OHdG, IL-1β, and IL-6 levels and TNF-α expression increased. Due to PdCl2 exposure, cytoprotective transcription factor Nrf2 expression decreased and caspase-3 expression increased. Along with the increase in ER stress (HSP70, HSP90, GRP78, and CHOP) induced by PdCl2, a decrease in aquaporin 1 and nephrin expressions was observed in renal tissues due to histopathological changes in hepatorenal tissues. Que treatment together with PdCl2 reduced PdCl2-induced hepatorenal toxicity and provided improvement in the investigated parameters.

摘要

为了解环境中分散的钯颗粒的潜在危害,需要进行全面的毒理学研究。槲皮素(Que)是一种具有抗氧化特性的天然黄酮类化合物。本研究旨在探讨使用Que(30 mg/kg体重)对氯化钯(PdCl2)(8 mg/kg体重)诱导的大鼠肝肾毒性中的氧化应激、细胞凋亡、炎症和内质网(ER)应激损伤的潜在保护作用。应用PdCl2 28天后,肝肾组织中的抗氧化能力(超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽S-转移酶)下降,脂质过氧化标志物丙二醛水平升高。此外,血清中谷丙转氨酶、谷草转氨酶、乳酸脱氢酶、尿素和肌酐等标志物也发生了变化。同样,对氧磷酶-1和乙酰胆碱酯酶活性下降,一氧化氮、8-羟基脱氧鸟苷、白细胞介素-1β和白细胞介素-6水平以及肿瘤坏死因子-α表达增加。由于暴露于PdCl2,细胞保护转录因子Nrf2表达下降,半胱天冬酶-3表达增加。随着PdCl2诱导的内质网应激(热休克蛋白70、热休克蛋白90、葡萄糖调节蛋白78和C/EBP同源蛋白)增加,由于肝肾组织的组织病理学变化,肾组织中水通道蛋白1和nephrin表达下降。Que与PdCl2联合治疗可降低PdCl2诱导的肝肾毒性,并使所研究的参数得到改善。

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