Ameliorative impacts of sinapic acid against mercuric chloride-induced renal toxicity: role of antioxidants and inflammatory cytokines.

IF 2.2 4区 医学 Q3 TOXICOLOGY Toxicology Research Pub Date : 2024-04-23 eCollection Date: 2024-04-01 DOI:10.1093/toxres/tfae066
Arshad Mehmood, Mohamed Mohamed Soliman, Daklallah A Almalki, Khalid S Alotaibi, Gehan Basiony Ahmed Youssef, Saed Althobaiti
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Abstract

Because of their beneficial properties, natural products, especially medicinal plants, are becoming increasingly popular worldwide and play a significant role in research. This study was aimed to evaluate the nephroprotective effect of sinapic acid against mercuric chloride-induced renal toxicity in mice. The mice were allocated to four groups named a normal group (G1), model group (G2; received HgCl2, 1 mg/kg bw), treatments groups (G3 and G4: received 50 and 100 mg/kg bw of sinapic acid together with HgCl2). Mice received HgCl2 remarkably showed alteration in all examined biochemical biomarkers (urea, creatinine, and bilirubin), and induced alteration in blood cell picture and anemia. HgCl2 intoxication decreased both systemic and renal antioxidant activity and induced over all oxidative stress as indicated by alteration in inflammation and oxidative stress associated markers. HgCl2 affected renal histology with leukocytic and inflammatory cell infiltration, fibrosis and tubular necrosis. Administration of sinapic acid (50 and 100 mg/kg bw) markedly restored the HgCl2-induced oxidative stress (serum and renal: MDA, GSH, CAT, SOD, and T-AOC), proinflammatory cytokines (serum and renal: TNF-α, IL-6, IL-1β, and PGE2) and restored the changes on biochemical markers, and hematological parameters (hemoglobin, erythrocytes, platelets, and leukocytes). Taken together, the results of the present study disclose that sinapic acid has the potential to attenuate HgCl2-induced renal toxicity and may be an ideal choice against mercury poisoning.

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西那皮酸对氯化汞诱发的肾毒性的改善作用:抗氧化剂和炎症细胞因子的作用
天然产品,尤其是药用植物,因其有益的特性,在全世界越来越受欢迎,并在研究中发挥着重要作用。本研究旨在评估山奈酸对氯化汞引起的小鼠肾毒性的保护作用。小鼠被分为四组,分别为正常组(G1)、模型组(G2;接受氯化汞治疗,1 毫克/千克体重)、治疗组(G3 和 G4:接受 50 和 100 毫克/千克体重的山奈酸和氯化汞治疗)。氯化汞中毒小鼠的所有生化指标(尿素、肌酐和胆红素)都发生了显著变化,并导致血细胞图谱改变和贫血。氯化汞中毒会降低全身和肾脏的抗氧化活性,诱发全面的氧化应激,炎症和氧化应激相关标志物的变化表明了这一点。氯化汞影响肾脏组织学,出现白细胞和炎症细胞浸润、纤维化和肾小管坏死。施用西那匹酸(50 和 100 毫克/千克体重)可显著恢复氯化汞诱导的氧化应激(血清和肾脏:MDA、GSH、CAT、SOD 和 T-AOC)、促炎细胞因子(血清和肾脏:TNF-α、IL-6、IL-1β 和 PGE2),并恢复生化指标和血液学参数(血红蛋白、红细胞、血小板和白细胞)的变化。综上所述,本研究的结果表明,西那皮酸具有减轻盐酸汞诱导的肾毒性的潜力,可能是防治汞中毒的理想选择。
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来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
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