Role of 17-β Estradiol and Ramipril in OPG/RANKL Pathway in a Rat Model of Post-Menopausal Osteoporosis

Khloussy, Hemmat Mohamed; Badawy, Ahmed Desouky; Mohamed, Yara Sayed Ibrahim Eldesouki; Maher, Muhammad

doi:10.21608/ejhm.2023.279677

Role of 17-β Estradiol and Ramipril in OPG/RANKL Pathway in a Rat Model of Post-Menopausal Osteoporosis

Document Type : Original Article

Authors

10.21608/ejhm.2023.279677

Abstract

Background: Primary osteoporosis and other metabolic bone disorders have been linked to the proteins osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL).
Aim and objectives: Our study's goal was to examine the effects of co-administering estradiol (E2) and ramipril (ACEI) on bone markers in ovariectomized rats and to assess the potential interactions between these medications in order to address the function of the OPG/RANKL system as a potential mechanism of action.
Materials and methods: 40 female rats, randomly divided into 5 groups, each group included 8 rats. · Group 1: Control group (sham operated). Group 2: Ovariectomized rats (OVX). Group 3: Ovariectomized rats (OVX)+E2. Group 4: Ovariectomized rats (OVX)+ACEI. Group 5: Ovariectomized rats (OVX)+E2+ACEI.
Results: OVX rats showed a significant decrease in serum Ca²⁺ and OPG levels with significant increase in serum RANKL, osteocalcin, alkaline phosphatase activity and urinary hydroxyproline levels compared to control group. Treatment with ramipril as well as E2 led to a significant improvement in bone markers levels with a significant increase in serum OPG level with a significant reduction in serum RANKL level compared to OVX group.
Conclusion: Ramipril as ACEI had more significant effect on decreasing serum bone markers level than 17-β estradiol in ovariectomized rats. So, we can draw the conclusion that altering OPG/RANKL signalling may be a possible mechanism by which E2 and ACEI prevent osteoporosis.

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