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白杨素对丙烯酰胺诱导的肝毒性的保护作用:对大鼠氧化应激、炎症、凋亡、自噬及组织学评估的见解

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

作者信息

Gencer Selman, Akaras Nurhan, Şimşek Hasan, Gür Cihan, İleritürk Mustafa, Küçükler Sefa, Kandemir Fatih Mehmet

机构信息

Department of Internal Diseases, Faculty of Medicine, Aksaray University, Aksaray, Turkey.

Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Turkey.

出版信息

J Biochem Mol Toxicol. 2025 Jun;39(6):e70334. doi: 10.1002/jbt.70334.

DOI:10.1002/jbt.70334
PMID:40488268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12147197/
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.

摘要

丙烯酰胺(ACR)是一种具有高致癌风险的有毒化学物质,它是在高温加热或加工食品过程中释放出来的。白杨素(CHR)是一种黄酮类化合物,天然存在于蜂蜜和西番莲等食物中,以其抗氧化、抗癌和抗炎特性而闻名。本研究旨在确定CHR对ACR诱导的肝毒性的保护作用。以38.27毫克/千克的剂量口服给予ACR;以25或50毫克/千克的剂量口服给予CHR,持续十天。采用生化和分子方法研究肝组织中的氧化应激、炎症和凋亡标志物。此外,采用组织学方法确定肝组织的结构和功能特征以及自噬情况。CHR治疗通过增加抗氧化剂(超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽)和降低升高的氧化剂丙二醛来减轻ACR诱导的氧化应激。CHR通过使核因子-κB和促炎细胞因子失活来降低炎症活性。CHR降低了ACR诱导的凋亡相关半胱天冬酶-3、半胱天冬酶-6、半胱天冬酶-9和Bax的增加,同时提高了抗凋亡蛋白Bcl-2降低的水平。免疫组织化学还确定CHR抑制自噬相关蛋白Beclin-1的活性。CHR在减轻ACR诱导的肝毒性损伤方面有效,可能是一种有效的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/a22dd6ecc642/JBT-39-e70334-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/a445de13962e/JBT-39-e70334-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/639e7ed49880/JBT-39-e70334-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/22a3c17e2578/JBT-39-e70334-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/d917fca3be11/JBT-39-e70334-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/a22dd6ecc642/JBT-39-e70334-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/a445de13962e/JBT-39-e70334-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/639e7ed49880/JBT-39-e70334-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/22a3c17e2578/JBT-39-e70334-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/d917fca3be11/JBT-39-e70334-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da76/12147197/a22dd6ecc642/JBT-39-e70334-g001.jpg

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本文引用的文献

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Bioimpacts. 2024 Jul 9;15:30269. doi: 10.34172/bi.30269. eCollection 2025.
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Naringin protects against paclitaxel-induced toxicity in rat testicular tissues by regulating genes in pro-inflammatory cytokines, oxidative stress, apoptosis, and JNK/MAPK signaling pathways.柚皮苷通过调节促炎细胞因子、氧化应激、细胞凋亡和 JNK/MAPK 信号通路中的基因来防止紫杉醇诱导的大鼠睾丸组织毒性。
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Chrysin mitigated neuropathic pain and peripheral sensitization in knee osteoarthritis rats by repressing the RAGE/PI3K/AKT pathway regulated by HMGB1.白杨素通过抑制由高迁移率族蛋白B1(HMGB1)调控的晚期糖基化终末产物受体(RAGE)/磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(AKT)通路,减轻膝骨关节炎大鼠的神经性疼痛和外周敏化。
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