Planta Med
DOI: 10.1055/s-0043-108761
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Tanshinol Alleviates Osteoporosis and Myopathy in Glucocorticoid-Treated Rats

Guanghua Chen1, *, Xinle Zhang2, *, Han Lin3, *, Guizhi Huang1, *, Yahui Chen2, Liao Cui2, 4
  • 1Department of Orthopedics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China
  • 2Department of Pharmacology, School of Pharmacy, Guangdong Medical University, Zhanjiang, Guangdong, China
  • 3Department of Orthopedics, Affiliated Hospital of Guizhou Medical University, Guian, Guizhou, China
  • 4Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical University, Zhanjiang, Guangdong, China
Further Information

Publication History

received 07 January 2017
revised 23 March 2017

accepted 02 April 2017

Publication Date:
20 April 2017 (eFirst)

Abstract

Tanshinol is a major water-soluble active component of Salvia miltiorrhiza. In this study, we aimed to investigate whether tanshinol has potential therapeutic effects against glucocorticoid-induced osteoporosis and glucocorticoid-induced myopathy. Ninety-six female Sprague-Dawley rats were randomly assigned to five groups: a control group, a model group, and three model groups treated with 25 or 50 mg/kg of tanshinol, or calcitriol. All model groups received prednisone acetate for 90 days to induce glucocorticoid-induced osteoporosis. Afterwards, all animals underwent a surgical procedure to induce bone defects at the right proximal tibia. Prednisone treatment was stopped after surgery, but tanshinol or calcitriol treatment was continued to the endpoint. At the experimental endpoint, compared to the model group, 25 mg/kg tanshinol could significantly reverse glucocorticoid-induced loss of bone mineral density by 12.5 %, while enhancing mechanical bone strength, causing a significant 11 % increase in trabecular number, and reducing trabecular separation by 28 %. In addition, tanshinol improved the bone microarchitecture and prevented glucocorticoid-induced bone loss by promoting bone formation and inhibiting bone resorption. Moreover, results of bone defect repair and muscle weight measurements revealed that tanshinol accelerated the bone fracture healing process and attenuated muscle atrophy caused by glucocorticoid. Furthermore, qRT-PCR analysis showed a 1-fold upregulation in mRNA levels of transforming growth factor beta and roughly 6-fold increases in vascular endothelial growth factor mRNA expression in calluses from the tanshinol groups. Tanshinol also preserved muscular ubiquitin mRNA levels from glucocorticoid-induced elevation. These findings demonstrate the potential benefits of tanshinol against glucocorticoid-induced osteoporosis and glucocorticoid-induced myopathy, which warrants further investigation in future studies.

* These authors contributed equally to this work.


Supporting Information