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水飞蓟素减轻双氯芬酸诱导的雄性Wistar大鼠肝毒性:组织病理学研究

Silymarin alleviates diclofenac-induced hepatotoxicity in male Wistar rats: Histopathological investigation.

作者信息

Alharbi Fawiziah Khalaf

机构信息

Department of Biology, College of Science, Buraydah, Qassim University, Buraydah, Saudi Arabia.

出版信息

Open Vet J. 2025 Apr;15(4):1790-1797. doi: 10.5455/OVJ.2025.v15.i4.31. Epub 2025 Apr 30.

DOI:10.5455/OVJ.2025.v15.i4.31
PMID:40453847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12124788/
Abstract

BACKGROUND

One of the primary concerns of the pharmaceutical industry is the potential for liver damage caused by drugs. Diclofenac is a member of the family of nonsteroidall anti-inflammatory medications, which are known for their anti-inflammatory, antipyretic, and analgesic effects. Although it is commonly prescribed, liver damage is one of the primary risks associated with this medication. Therefore, it is necessary to use a prospective therapeutic medication that can counteract the cytotoxic impact of diclofenac. Humans have utilized natural items as a means of obtaining sustenance, maintaining their health, and treating a wide variety of illnesses. Antioxidant, anti-inflammatory, and liver-protective properties are associated with , which is a flavonoid chemical derived from the seeds of the marianum plant.

AIM

This study aimed to evaluate the possible hepatoprotective effect of silymarin against diclofenac-induced liver injury.

METHODS

Forty Wistar rats were used in the current investigation and grouped randomly into four equal groups. The first group (G1) was kept as a control group. G2 received intraperitoneal injections of diclofenac (50 mg/kg. BW/day) for 5 days. G3 received oral silymarin for 5 days (200 mg/kg BW/day) dissolved in distal water. G4 received diclofenac plus silymarin with the same previously mentioned doses for 5 days. The animals were collected and subjected to histopathological examination.

RESULTS

The diclofenac-treated group showed several pathological changes within the hepatic parenchyma, including diffuse coagulative and hydropic degenerations with general disorganization of the hepatic cords, severe dilatation and congestion of the central vein and portal blood vessels, severe sinusoidal dilatation and congestions accompanied with severe pressure atrophy of the hepatic cords, and severe inflammatory cell infiltrations. Meanwhile, the diclofenac plus silymarin-treated group showed a significant good effect, where silymarin ameliorated almost all histopathological lesions induced after diclofenac treatment as mitigating the degenerative changes of hepatocytes, minimizing inflammatory cell infiltrations, and normal organized hepatic rays with normal sinusoids in between were distinguished.

CONCLUSION

Silymarin has a significant hepatoprotective effect against diclofenac-induced hepatotoxicity through neutralization of all histopathological injuries.

摘要

背景

制药行业主要关注之一是药物引起肝损伤的可能性。双氯芬酸是非甾体抗炎药物家族的一员,以其抗炎、解热和镇痛作用而闻名。尽管它是常用药物,但肝损伤是与此药物相关的主要风险之一。因此,有必要使用一种前瞻性治疗药物来对抗双氯芬酸的细胞毒性影响。人类利用天然物品作为获取食物、维持健康和治疗各种疾病的一种方式。水飞蓟素是一种从水飞蓟植物种子中提取的类黄酮化合物,具有抗氧化、抗炎和肝脏保护特性。

目的

本研究旨在评估水飞蓟素对双氯芬酸诱导的肝损伤可能的肝保护作用。

方法

本研究使用40只Wistar大鼠,随机分为四个相等的组。第一组(G1)作为对照组。G2腹腔注射双氯芬酸(50mg/kg体重/天),持续5天。G3口服水飞蓟素5天(200mg/kg体重/天),溶于去离子水中。G4接受双氯芬酸加水飞蓟素,剂量与上述相同,持续5天。收集动物并进行组织病理学检查。

结果

双氯芬酸治疗组肝实质内出现了几种病理变化,包括弥漫性凝固性和水样变性,肝索普遍紊乱,中央静脉和门静脉严重扩张和充血,严重的肝血窦扩张和充血,伴有肝索严重压迫性萎缩,以及严重的炎性细胞浸润。同时,双氯芬酸加水飞蓟素治疗组显示出显著的良好效果,水飞蓟素改善了双氯芬酸治疗后几乎所有的组织病理学损伤,如减轻肝细胞的变性变化、减少炎性细胞浸润,并且可区分出正常排列的肝索和其间正常的肝血窦。

结论

水飞蓟素通过中和所有组织病理学损伤,对双氯芬酸诱导的肝毒性具有显著的肝保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/7894d21564d9/OpenVetJ-15-1790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/f25f32b39f56/OpenVetJ-15-1790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/e1b4f928f012/OpenVetJ-15-1790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/8a3ce6a4bc88/OpenVetJ-15-1790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/7894d21564d9/OpenVetJ-15-1790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/f25f32b39f56/OpenVetJ-15-1790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/e1b4f928f012/OpenVetJ-15-1790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/8a3ce6a4bc88/OpenVetJ-15-1790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8130/12124788/7894d21564d9/OpenVetJ-15-1790-g004.jpg

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