Format

Send to

Choose Destination
Biomed Pharmacother. 2019 Feb;110:895-905. doi: 10.1016/j.biopha.2018.11.004. Epub 2018 Dec 17.

Rosuvastatin attenuates piroxicam-mediated gastric ulceration and hepato-renal toxicity in rats.

Author information

1
Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt. Electronic address: ahmed.abdeen@fvtm.bu.edu.eg.
2
Department of Pharmacology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt.
3
Department of Pharmacology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt; Benha University Hospital, Faculty of Medicine, Benha University, Benha 13518, Egypt.
4
Department of Anatomy and Embryology, Faculty of Veterinary Medicine, University of Sadat City, Menoufia, 22857, Egypt.
5
Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Benha University, Benha 13518, Egypt.
6
Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Benha University, Toukh 13736, Egypt.

Abstract

Piroxicam (Px) is a non-steroidal anti-inflammatory drug that is widely prescribed in various inflammatory disorders. However, Px is known to induce gastric ulceration and hepato-renal toxicity. Rosuvastatin (ROSV), a member of the statin family, has anti-inflammatory and antioxidant actions independent of its anti-hyperlipidemic action. Therefore, we investigated the protective effects of ROSV against Px-induced gastric, liver, and kidney injury. Five groups of seven rats each were used; control group, ROSV group (20 mg/kg, given orally), Px group (7 mg/kg, given intraperitoneally), Px+ROSV L (7 and 10 mg/kg, respectively), and Px+ROSV H (7 and 20 mg/kg, respectively) group. The results revealed that Px induced severe gastric mucosal damage expressed by high ulcer index along with significant increases in liver and kidney function parameters including AST, ALT, creatinine, and urea. Disrupted lipid metabolism also was observed in Px-treated animals. Moreover, marked an increase in malondialdehyde (MDA) and decreases in glutathione (GSH) and catalase (CAT) levels along with enhanced activated caspase-3 expression in the gastric, hepatic, and renal tissues following Px-insult suggested a possible involvement of lipid peroxidation in Px-induced gastropathy and hepatorenal toxicity. However, in a dose-dependent manner, ROSV was able to mitigate Px-induced lipid peroxidation and apoptosis in gastric, liver, and kidney tissues.

KEYWORDS:

Apoptosis; Gastric ulcer; Hepato-renal toxicity; Lipid peroxidation; Piroxicam; Rosuvastatin

PMID:
30572194
DOI:
10.1016/j.biopha.2018.11.004
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center