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厚朴酚通过信号通路减轻环磷酰胺诱导的氧化应激、炎症和细胞凋亡。

Magnolin alleviates cyclophosphamide-induced oxidative stress, inflammation, and apoptosis via signaling pathway.

作者信息

Ince Sinan, Demirel Hasan Huseyin, Demirkapi Ezgi Nur, Kucukkurt Ismail, Eryavuz Abdullah, Arslan-Acaroz Damla, Acaroz Ulas, Tureyen Ali

机构信息

Faculty of Veterinary Medicine, Department of Pharmacology and Toxicology, Afyon Kocatepe University, 03200 Afyonkarahisar, Turkey.

Bayat Vocational School, Afyon Kocatepe University, 03780 Afyonkarahisar, Turkey.

出版信息

Toxicol Res (Camb). 2024 Aug 14;13(4):tfae129. doi: 10.1093/toxres/tfae129. eCollection 2024 Aug.

DOI:10.1093/toxres/tfae129
PMID:39148957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11323662/
Abstract

In the present study, we investigated the protective effect of magnolin (MAG) against oxidative stress induced by cyclophosphamide (CP) and its role in the signaling pathway. Rats were administered MAG (1 mg/kg, i.p.) for 14 days and CP (75 mg/kg, i.p.) on the 14th day. CP administration increased tissue damage, as evidenced by elevated levels of transaminases (aspartate and alanine), alkaline phosphatase, and renal parameters (blood urea nitrogen and creatinine). Additionally, 8-hydroxy-2'-deoxyguanosine and malondialdehyde levels were increased, whereas glutathione levels, along with catalase and superoxide dismutase activities, decreased in CP-treated rats. CP also down-regulated the expression of and , while up-regulating α and in liver and kidney tissues. In addition, CP treatment caused histopathological changes in heart, lung, liver, kidney, brain, and testis tissues. Treatment with MAG improved biochemical and oxidative stress parameters and prevented histopathological changes in CP-treated rats. Moreover, MAG suppressed the expression of inflammatory cytokines and apoptosis markers. In conclusion, MAG effectively prevented CP-induced toxicity by reducing oxidative stress, inflammation, and apoptosis, with its protective efficacy associated with the up-regulation of signaling.

摘要

在本研究中,我们研究了厚朴酚(MAG)对环磷酰胺(CP)诱导的氧化应激的保护作用及其在信号通路中的作用。大鼠连续14天腹腔注射MAG(1毫克/千克),并在第14天腹腔注射CP(75毫克/千克)。CP给药增加了组织损伤,这通过转氨酶(天冬氨酸和丙氨酸)、碱性磷酸酶和肾脏参数(血尿素氮和肌酐)水平的升高得以证明。此外,在CP处理的大鼠中,8-羟基-2'-脱氧鸟苷和丙二醛水平升高,而谷胱甘肽水平以及过氧化氢酶和超氧化物歧化酶活性降低。CP还下调了肝脏和肾脏组织中[此处原文缺失具体基因名称]和[此处原文缺失具体基因名称]的表达,同时上调了α和[此处原文缺失具体基因名称]的表达。此外,CP处理导致心脏、肺、肝脏、肾脏、大脑和睾丸组织出现组织病理学变化。MAG处理改善了CP处理大鼠的生化和氧化应激参数,并预防了组织病理学变化。此外,MAG抑制了炎性细胞因子和凋亡标志物的表达。总之,MAG通过降低氧化应激、炎症和凋亡有效地预防了CP诱导的毒性,其保护作用与[此处原文缺失具体信号通路名称]信号的上调有关。

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