The Protective Effects of Chrysin on Acrylamide-Induced Hepatotoxicity: Insights Into Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histological Evaluation in Rats

IF 3.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Selman Gencer, Nurhan Akaras, Hasan Şimşek, Cihan Gür, Mustafa İleritürk, Sefa Küçükler, Fatih Mehmet Kandemir
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Abstract

Acrylamide (ACR) is a toxic chemical with a high carcinogenic risk that is released as a result of heating or processing foods at high temperatures. Chrysin (CHR) is a flavonoid that is naturally found in foods such as honey and passionflower and stands out with its antioxidant, anticancer, and anti-inflammatory properties. This study aims to determine the protective effects of CHR in ACR-induced hepatotoxicity. ACR was administered orally at a dose of 38.27 mg/kg; CHR (25 or 50 mg/kg) was administered orally for ten days. Biochemical and molecular methods were used to investigate oxidative stress, inflammation, and apoptotic markers in liver tissue. Additionally, histological methods were used to determine the liver tissue's structural and functional characteristics and autophagy. CHR treatment alleviated ACR-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased oxidant MDA. CHR reduced inflammatory activity by inactivating NF-κB and pro-inflammatory cytokines. ACR-induced increases in apoptotic Casp-3, Casp-6, Casp-9, and Bax were reduced by CHR, while the decreased level of antiapoptotic Bcl-2 was increased. It was also determined immunohistochemically that CHR inhibited autophagic Beclin-1 activity. CHR was effective in reducing ACR-induced hepatotoxicity damage and may be an effective treatment option.

Abstract Image

菊花素对丙烯酰胺引起的肝毒性的保护作用:氧化应激、炎症、细胞凋亡、自噬和大鼠组织学评价的见解
丙烯酰胺(ACR)是一种具有高致癌风险的有毒化学物质,在高温下加热或加工食品时会释放出来。黄菊花素(CHR)是一种类黄酮,天然存在于蜂蜜和西番莲等食物中,具有抗氧化、抗癌和抗炎的特性。本研究旨在确定CHR对acr诱导的肝毒性的保护作用。口服ACR,剂量为38.27 mg/kg;口服CHR(25或50 mg/kg) 10天。采用生化和分子方法研究肝组织氧化应激、炎症和凋亡标志物。此外,采用组织学方法测定肝组织的结构和功能特征以及自噬情况。CHR处理通过增加抗氧化剂(SOD、CAT、GPx、GSH)和降低氧化剂MDA的升高来缓解acr诱导的氧化应激。CHR通过使NF-κB和促炎细胞因子失活来降低炎症活性。CHR可降低acr诱导的凋亡蛋白Casp-3、Casp-6、Casp-9和Bax的升高,而抗凋亡蛋白Bcl-2的升高。免疫组织化学也证实CHR抑制Beclin-1自噬活性。CHR可有效减少acr引起的肝毒性损害,可能是一种有效的治疗选择。
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来源期刊
CiteScore
5.80
自引率
2.80%
发文量
277
审稿时长
6-12 weeks
期刊介绍: The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
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