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Protective effects of morin against acrylamide-induced hepatotoxicity and nephrotoxicity: A multi-biomarker approach.
Food and Chemical Toxicology ( IF 3.9 ) Pub Date : 2020-02-14 , DOI: 10.1016/j.fct.2020.111190
Fatih Mehmet Kandemir 1 , Serkan Yıldırım 2 , Sefa Kucukler 1 , Cuneyt Caglayan 3 , Ekrem Darendelioğlu 4 , Muhammet Bahaeddin Dortbudak 2
Affiliation  

Acrylamide (ACR) is a heat-induced carcinogen substance that is found in some foods due to cooking or other thermal processes. The aim of present study was to assess the probable protective effects of morin against ACR-induced hepatorenal toxicity in rats. The rats were treated with ACR (38.27 mg/kg b.w., p.o.) alone or with morin (50 and 100 mg/kg b.w., p.o.) for 10 consecutive days. Morin treatment attenuated the ACR-induced liver and kidney tissue injury by diminishing the serum AST, ALP, ALT, urea and creatinine levels. Morin increased activities of SOD, CAT and GPx and levels of GSH, and suppressed lipid peroxidation in ACR induced tissues. Histopathological changes and immunohistochemical expressions of p53, EGFR, nephrin and AQP2 in the ACR-induced liver and kidney tissues were decreased after administration of morin. In addition, morin reversed the changes in levels of apoptotic, autophagic and inflammatory parameters such as caspase-3, bax, bcl-2, cytochrome c, beclin-1, LC3A, LC3B, p38α MAPK, NF-κB, IL-1β, IL-6, TNF-α and COX-2 in the ACR-induced toxicity. Morin also affected the protein levels by regulating the PI3K/Akt/mTOR signaling pathway and thus alleviated ACR-induced apoptosis and autophagy. Overall, these findings may shed some lights on new approaches for the treatment of ACR-induced hepatotoxicity and nephrotoxicity.

中文翻译:

茉莉对丙烯酰胺诱导的肝毒性和肾毒性的保护作用:一种多生物标志物方法。

丙烯酰胺(ACR)是一种热诱导的致癌物质,由于烹饪或其他热处理而在某些食品中发现。本研究的目的是评估香豆素对大鼠ACR诱导的肝肾毒性的保护作用。大鼠单独接受ACR(38.27 mg / kg bw,口服)或马林(50和100 mg / kg bw,口服)连续10天。Morin治疗通过降低血清AST,ALP,ALT,尿素和肌酐水平来减轻ACR诱导的肝肾组织损伤。桑色素增加了SOD,CAT和GPx的活性以及GSH的水平,并抑制了ACR诱导的组织中的脂质过氧化。施用rinin后,ACR诱导的肝和肾组织中p53,EGFR,nephrin和AQP2的组织病理学变化和免疫组化表达降低。此外,莫林逆转了凋亡,自噬和炎症参数水平的变化,例如caspase-3,bax,bcl-2,细胞色素c,beclin-1,LC3A,LC3B,p38αMAPK,NF-κB,IL-1β,IL-6 ,TNF-α和COX-2在ACR中诱导毒性。桑色素还通过调节PI3K / Akt / mTOR信号通路来影响蛋白质水平,从而减轻了ACR诱导的细胞凋亡和自噬。总体而言,这些发现可能为治疗ACR引起的肝毒性和肾毒性的新方法提供了一些启示。桑色素还通过调节PI3K / Akt / mTOR信号通路来影响蛋白质水平,从而减轻了ACR诱导的细胞凋亡和自噬。总体而言,这些发现可能为治疗ACR引起的肝毒性和肾毒性的新方法提供了一些启示。桑色素还通过调节PI3K / Akt / mTOR信号通路来影响蛋白质水平,从而减轻了ACR诱导的细胞凋亡和自噬。总体而言,这些发现可能为治疗ACR引起的肝毒性和肾毒性的新方法提供了一些启示。
更新日期:2020-02-20
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