Effect of pigment epithelium-derived factor on prostaglandin E2 receptors (EP2/EP4) in glucocorticoid-induced osteoporosis in rats
JOURNAL OF PHARMACY AND PHARMACOLOGY, vol.78, no.2, 2026 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 78 Issue: 2
- Publication Date: 2026
- Doi Number: 10.1093/jpp/rgaf102
- Journal Name: JOURNAL OF PHARMACY AND PHARMACOLOGY
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE
- Ataturk University Affiliated: Yes
Abstract
Objectives This study investigated the effects of pigment epithelium-derived factor (PEDF) on bone homeostasis in a glucocorticoid-induced osteoporosis (GIOP) rat model, focusing on prostaglandin E2 receptors EP2 and EP4.Methods Male Sprague-Dawley rats were divided into six groups. Dexamethasone (DEX, 1 mg/kg) was administered intramuscularly twice weekly for 90 days to induce osteoporosis. PEDF (50, 100, 200 mg/kg) was then given subcutaneously for 30 days. Bone mineral density (BMD) and bone morphology were assessed by computed tomography. Bone turnover markers-C-terminal telopeptide of type I collagen (CTX-1), tartrate-resistant acid phosphatase 5b (TRAP-5b), and bone-specific alkaline phosphatase-as well as EP2/EP4 mRNA expressions were evaluated using qRT-PCR.Key findings Immunohistochemical analysis was performed for ALP, osteopontin, osteocalcin, and VEGFR1. PEDF partially mitigated DEX-induced weight loss and dose-dependently restored BMD. Histopathological analyses showed improved bone architecture in all PEDF-treated groups. PEDF increased bone formation markers, reduced bone resorption markers, and upregulated EP2/EP4 expression.Conclusion These findings indicate that PEDF exerts protective effects against GIOP and may modulate bone metabolism through EP2/EP4 signalling pathways. PEDF shows promise as a potential therapeutic agent for preventing bone loss in GIOP.