Al-Hayder Manal N, Aledani Tamadir H W, Al-Mayyahi Rawaa S
Department of Pharmacology and Toxicology, College of Pharmacy, University of Basrah, Basrah, Iraq.
Department of Clinical Laboratory Sciences, College of Pharmacy, University of Basrah, Basrah, Iraq.
J Taibah Univ Med Sci. 2021 Dec 13;17(4):715-723. doi: 10.1016/j.jtumed.2021.11.003. eCollection 2022 Aug.
Despite the various clinical benefits of nonsteroidal anti-inflammatory drugs, their frequent and prolonged use has led to numerous health risks, including hepatotoxicity. Hepatotoxicity mediated by oxidative stress can affect the lipid profile. The objective was to investigate whether post-treatment with vitamin C can ameliorate the effects of diclofenac and naproxen in the livers of prepubertal rats and to highlight their relationship with lipid profile.
Forty prepubertal female albino rats were distributed among the control group, the diclofenac-administered group (5 mg/kg/day), and the naproxen-administered group (50 mg/kg/day). This study included two phases. In Phase 1, only five rats from each group were dissected after 21 days of oral administration to assess the hepatotoxic effects of nonsteroidal drugs. In Phase 2, five of the remaining animals in each intervention group were post-treated with 25 mg/kg/day of vitamin C for an additional 21 days. After the administration and post-treatment, serum biochemical parameters and histopathological signs were evaluated.
Extreme elevation in the levels of aspartate and alanine aminotransferases was observed in the diclofenac and naproxen groups compared with those in the control ( < 0.001). In addition, the levels of high- and low-density lipoproteins were significantly impacted in these drug groups ( < 0.01, < 0.05 respectively). Several pathological signs in the liver histology were observed in both drug groups. After post-treatment with vitamin C, noticeable amelioration of these alterations was observed. There were slightly elevation in the liver enzymes and insignificant increase and decrease in the high and low-density lipoproteins respectively.
Vitamin C post-treatment ameliorated the hepatotoxicity induced by diclofenac sodium and naproxen.
尽管非甾体抗炎药具有多种临床益处，但其频繁和长期使用已导致众多健康风险，包括肝毒性。由氧化应激介导的肝毒性可影响血脂水平。本研究旨在探讨维生素C治疗后是否能改善双氯芬酸和萘普生对青春期前大鼠肝脏的影响，并突出它们与血脂水平的关系。
将40只青春期前雌性白化大鼠分为对照组、双氯芬酸给药组（5毫克/千克/天）和萘普生给药组（50毫克/千克/天）。本研究包括两个阶段。在第1阶段，口服给药21天后，每组仅解剖5只大鼠，以评估非甾体药物的肝毒性作用。在第2阶段，每个干预组的其余5只动物用25毫克/千克/天的维生素C进行后续治疗，持续21天。给药和后续治疗后，评估血清生化参数和组织病理学特征。
与对照组相比，双氯芬酸和萘普生组的天冬氨酸和丙氨酸转氨酶水平极度升高（<0.001）。此外，这些药物组的高密度和低密度脂蛋白水平也受到显著影响（分别为<0.01，<0.05）。在两个药物组的肝脏组织学中均观察到若干病理特征。用维生素C进行后续治疗后，这些改变得到明显改善。肝酶略有升高，高密度和低密度脂蛋白分别有不显著的增加和降低。
维生素C后续治疗改善了双氯芬酸钠和萘普生诱导的肝毒性。
