Alsubaie Nawal, Abd-Elhakim Yasmina M, Mohamed Amany Abdel-Rahman, Metwally Mohamed M M, Khamis Tarek, Eskandrani Areej A, Bawahab Ahmed Abdulwahab, Alotaibi Badriyah S, Ibrahim Rowida E
Department of Pharmacy Practice, College of Pharmacy, Princess Nourah bint Abdulrahman University, P.O. Box 84428, Riyadh, 11671, Saudi Arabia.
Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Zagazig University, Zagazig, 44519, Egypt.
Vet Res Commun. 2025 Jun 13;49(4):223. doi: 10.1007/s11259-025-10779-9.
Cadmium (Cd²⁺) contamination severely threatens aquatic organisms, leading to oxidative stress, inflammation, and hepatotoxicity. Portulaca oleracea is known for its antioxidant and anti-inflammatory activities; yet, its defensive role against Cd²⁺-induced hepatotoxicity in Nile tilapia (Oreochromis niloticus) is still unclear. The current study evaluated the possible hepatoprotective effects of purslane leaf powder (PR) against Cd²⁺-induced liver damage and its mechanisms. A hepatotoxicity model was established by exposing tilapia to Cd²⁺ (50 µg/L) for 60 days, with and without PR supplementation (10 g PR/kg diet). Histopathological analysis, biochemical assays, and real-time quantitative PCR were done to assess liver tissue damage, oxidative stress markers, lipid profile, and inflammatory gene expression. Results showed that Cd²⁺ exposure induced severe hepatic alterations, including glycogen depletion, steatosis, necrosis, and inflammatory infiltration, along with increased liver indices and obvious dyslipidemia. PR supplementation significantly alleviated these changes by reducing oxidative stress, enhancing antioxidant enzyme activity, upregulating antioxidant genes (sod-1, sod-2, cat, gpx, and cyp1a), and downregulating inflammatory markers (mapk1, nf-κb, il1β, il6, il8, and tnf-α). Additionally, PR improved lipid profile and liver morphology, and reduced hepatocyte damage compared to the Cd²-exposed group. In conclusion, PRP mitigates Cd²⁺-induced hepatotoxicity in Nile tilapia by enhancing antioxidant defenses and reducing inflammation, suggesting its potential as a dietary supplement to counteract heavy metal toxicity in aquaculture.
镉（Cd²⁺）污染严重威胁水生生物，导致氧化应激、炎症和肝毒性。马齿苋以其抗氧化和抗炎活性而闻名；然而，其对尼罗罗非鱼（Oreochromis niloticus）中Cd²⁺诱导的肝毒性的防御作用仍不清楚。本研究评估了马齿苋叶粉（PR）对Cd²⁺诱导的肝损伤的可能肝脏保护作用及其机制。通过将罗非鱼暴露于Cd²⁺（50 μg/L）60天建立肝毒性模型，同时添加或不添加PR（10 g PR/kg饲料）。进行了组织病理学分析、生化测定和实时定量PCR，以评估肝组织损伤、氧化应激标志物、脂质谱和炎症基因表达。结果表明，Cd²⁺暴露诱导了严重的肝脏改变，包括糖原耗竭、脂肪变性、坏死和炎症浸润，同时肝脏指数增加和明显的血脂异常。补充PR通过降低氧化应激、增强抗氧化酶活性、上调抗氧化基因（sod-1、sod-2、cat、gpx和cyp1a）以及下调炎症标志物（mapk1、nf-κb、il1β、il6、il8和tnf-α）显著减轻了这些变化。此外，与Cd²⁺暴露组相比，PR改善了脂质谱和肝脏形态，并减少了肝细胞损伤。总之，PRP通过增强抗氧化防御和减轻炎症减轻了尼罗罗非鱼中Cd²⁺诱导的肝毒性，表明其作为水产养殖中对抗重金属毒性的膳食补充剂的潜力。
