Autophagy, SMAD-1, and apoptotic pathways are correlated with L-carnitine protective effect against dexamethasone-induced osteoporosis in Wistar rats | ||||
| Records of Pharmaceutical and Biomedical Sciences | ||||
| Article 13, Volume 6, Issue 3, April 2022, Page 148-164 PDF (1.05 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/rpbs.2022.150356.1155 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Sanaa Ahmed  1; Dalia Elbahy2
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| 1department of pharmacology Faculty of Medicine Sohag University Egypt. | ||||
| 2Department of Pharmacology, Faculty of Medicine, Sohag University, Sohag, Egypt | ||||
| Abstract | ||||
| Background: Osteoporosis (O.P) is a metabolic bone disease characterized by bone mass loss and bone weakness. The cofactor in fatty acid beta-oxidation, L-carnitine (L-C), has been found to regulate osteoblast activity. Therefore, this work aimed to investigate the potential defensive properties of L-C versus dexamethasone (DEXA) induced O.P, as well as the underlying mechanisms. Methods: Thirty female Wistar rats were divided randomly into three equal groups (n = 10). The control group: received saline throughout the study; the DEXA-treated group: received DEXA (7 mg/kg/week) I.M. for four successive weeks; the L-C + DEXA treated group: received L-C (100 mg/kg/day, orally) for two weeks followed by L-C+ DEXA for a further four successive weeks simultaneously in the same previous doses and routes. Results: L-C treatment attenuated the decline in femur and body weights, calcium, osteoprotegerin (OPG), and total antioxidant capacity resulting from DEXA administration. In contrast, L-C ameliorated DEXA-induced elevation in alkaline phosphatase and oxidative stress. Furthermore, L-C reduced the expression of an apoptosis-related gene; caspase-3, however, augmented the expression of autophagy-related genes ATG-5 and Smad-1 in rat bone. Histopathological findings further supported the protective effects of LC against DEXA-induced O.P. Conclusion: The current study findings demonstrated the protective effects of L-C on DEXA-induced O.P due to the reduction of oxidative stress, apoptosis, and increasing autophagy and smad-1 protein gene expression. Consequently, L-C can be used as an additive in the treatment of O.P. | ||||
| Keywords | ||||
| Apoptosis; Autophagy; Bone mineral density; Osteoporosis; L-carnitine | ||||
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