Didymin protects against polystyrene nanoplastic-induced hepatic damage in male albino rats by modulation of Nrf-2/Keap-1 pathway

IF 17.7 1区 化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2024-01-22 DOI:10.1590/1414-431X2023e13173
M.U. Ijaz, N. Nadeem, A. Hamza, M.H. Almutairi, U. Atique
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Abstract

Polystyrene nanoplastics (PS-NPs) are ubiquitous environmental pollutants that can cause oxidative stress in various organs, including the liver. Didymin is a dietary flavanone that displays multiple pharmacological activities. Therefore, the present study evaluated the palliative role of didymin against PS-NPs-induced hepatic damage in rats. Albino rats (n=48) were randomly distributed into 4 groups: control, PS-NPs treated group, PS-NPs + didymin co-administered group, and didymin supplemented group. After 30 days, PS-NPs intoxication lowered the expression of Nrf-2 and anti-oxidant genes [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR), glutathione-S-transferase (GST), and heme oxygenase-1 (HO-1)], whereas the expression of KEAP1 kelch like ECH associated protein 1 (Keap-1) was increased. PS-NPs exposure also reduced the activities of anti-oxidants enzymes (CAT, SOD, GPx, GSR, GST, GSH, and OH-1), while malondialdehyde (MDA) and reactive oxygen species (ROS) levels were increased. The levels of alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were increased in PS-NPs-exposed rats. Moreover, inflammatory indices [interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), nuclear factor-kappa B (NF-κB), and cyclooxygenase-2 (COX-2)] were increased in PS-NPs-exposed rats. Furthermore, PS-NPs intoxication increased the expressions of apoptotic markers including Bax and Caspase-3, as well as reducing Bcl-2 expression. The histopathological analysis showed significant damage in PS-NPs-treated rats. However, didymin supplementation ameliorated all the PS-NPs-induced damage in the liver of rats. Therefore, it was concluded that didymin can act as a remedy against PS-NPs-induced liver toxicity due to its anti-apoptotic, anti-oxidant, and anti-inflammatory activities.
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地迪明通过调节 Nrf-2/Keap-1 通路保护雄性白化大鼠免受聚苯乙烯纳米塑料诱发的肝损伤
聚苯乙烯纳米塑料(PS-NPs)是一种无处不在的环境污染物,可对包括肝脏在内的多个器官造成氧化应激。Didymin是一种膳食黄酮,具有多种药理活性。因此,本研究评估了地迪明对 PS-NPs 引起的大鼠肝损伤的缓解作用。将白化大鼠(n=48)随机分为 4 组:对照组、PS-NPs 处理组、PS-NPs + 稻瘟灵合用组和补充稻瘟灵组。30天后,PS-NPs中毒降低了Nrf-2和抗氧化基因[过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GSR)、谷胱甘肽-S-转移酶(GST)和血红素加氧酶-1(HO-1)]的表达,而KEAP1 kelch like ECH associated protein 1(Keap-1)的表达增加。接触 PS-NPs 还降低了抗氧化酶(CAT、SOD、GPx、GSR、GST、GSH 和 OH-1)的活性,同时丙二醛(MDA)和活性氧(ROS)水平升高。暴露于 PS-NPs 的大鼠体内的丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)和碱性磷酸酶(ALP)水平均有所升高。此外,PS-NPs 暴露大鼠的炎症指数[白细胞介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、核因子-Kappa B(NF-κB)和环氧化酶-2(COX-2)]也有所增加。此外,PS-NPs 中毒增加了包括 Bax 和 Caspase-3 在内的凋亡标志物的表达,同时降低了 Bcl-2 的表达。组织病理学分析表明,PS-NPs 对大鼠造成了明显的损伤。然而,补充地迪明后,大鼠肝脏中所有由 PS-NPs 引起的损伤都得到了改善。因此,可以得出结论:由于具有抗细胞凋亡、抗氧化和抗炎活性,didymin 可以作为一种治疗 PS-NPs 引起的肝脏毒性的药物。
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来源期刊
Accounts of Chemical Research
Accounts of Chemical Research 化学-化学综合
CiteScore
31.40
自引率
1.10%
发文量
312
审稿时长
2 months
期刊介绍: Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.
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