关键词: NLRP3 inflammasome apoptose apoptosis autophagie autophagy contrast-induced nephropathy inflammasome NLRP3 melatonin mélatonine néphropathie entraînée par les produits de contraste

Mesh : Acute Kidney Injury / chemically induced prevention & control Animals Apoptosis Autophagy Biomarkers Contrast Media Inflammasomes Inflammation / pathology Male Melatonin / pharmacology therapeutic use NLR Family, Pyrin Domain-Containing 3 Protein Rats

来  源:   DOI:10.1139/cjpp-2022-0111

Abstract:
Contrast medium (CM) is a chemical substance that is used for imaging anatomical boundaries and to explore normal and abnormal physiological findings; the use of CM was associated with kidney injury and acute renal failure. Melatonin (M) possesses antioxidant, anti-inflammatory, and antiapoptotic effects in addition to autophagy modulation. This study aimed to investigate the protective effect of M against contrast-induced nephropathy (CIN) and its impact on the crosstalk between inflammasome, apoptosis, and autophagy in CIN. Male albino rats received M (10, 20, and 40 mg/kg/day, intraperitoneally) for 3 days. One hour after the last administration, rats were subjected to CIN induction (10 mg/kg indomethacin, double doses of l-NAME 10 mg/kg, i.v., and meglumine diatrizoate 60% 6 mL/kg, i.v.). CIN-induced kidney damage was evidenced through elevated kidney function biomarkers and induced renal histopathological changes. Pretreatment with M caused a significant decrease in nephrotoxicity biomarkers and histopathological alterations. Moreover, CIN-induced oxidative stress, NLRP3 inflammasome, and apoptosis were attenuated by M. Furthermore, M modulates autophagy in CIN rats. M inhibits CIN-induced NLRP3-inflammasome activation and apoptosis as well as enhances autophagy.
摘要:
造影剂(CM)是一种用于成像解剖边界并探索正常和异常生理发现的化学物质;CM的使用与肾损伤和急性肾衰竭有关。褪黑素(M)具有抗氧化剂,抗炎,以及自噬调节之外的抗凋亡作用。本研究旨在探讨M对对比剂肾病(CIN)的保护作用及其对炎症小体串扰的影响。凋亡,和自噬在CIN.雄性白化病大鼠接受M(10、20和40mg/kg/天,腹膜内)3天。上次政府一小时后,大鼠接受CIN诱导(10mg/kg吲哚美辛,双倍剂量的l-NAME10mg/kg,i.v.,和泛影葡胺60%6mL/kg,i.v.).CIN诱导的肾损伤通过升高的肾功能生物标志物和诱导的肾组织病理学改变得到证实。用M预处理导致肾毒性生物标志物和组织病理学改变的显着减少。此外,CIN诱导的氧化应激,NLRP3炎性体,细胞凋亡被M.M在CIN大鼠中调节自噬。M抑制CIN诱导的NLRP3炎性体激活和凋亡,并增强自噬。
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