Involvement of PI3K/Akt/β-catenin signaling in schisandrin B-mitigated bone deterioration in an experimental rat model of estrogen deficiency
Wei Li 2
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Department of Orthopedics, The First People’s Hospital of Taizhou, Taizhou, China
The Second Clinical School of North Sichuan Medical College, Nanchong, China
Department of Spine Surgery, Affiliated Hospital of Yanbian University, Yanji, China
Submission date: 2019-07-10
Final revision date: 2019-09-20
Acceptance date: 2019-10-02
Online publication date: 2020-02-11
Schisandrin B (SchB) has been reported to perform a wide range of biological functions, including antioxidant activity, anti-inflammatory activity and stimulation of osteoblast proliferation. However, the function and mechanism of SchB in ovariectomy (OVX)-induced osteoporosis are still unknown. The present study was designed to investigate the anti-osteoporotic activity of SchB in an experimental rat model of estrogen deficiency, which is usually used to mimic human postmenopausal osteoporosis (PMO).

Material and methods:
OVX rats were orally treated with low (10 mg/kg) or high (50 mg/kg) doses of SchB for 8 weeks. Bone metabolism-related markers were measured by ELISA. The levels of protein expression were determined by western blotting analysis. Hematoxylin and eosin (H&E) and safranin O staining were performed to analyze trabecular bone and cartilage degeneration. Tartrate-resistant acid phosphatase (TRAP) staining was used to evaluate osteoclast differentiation.

SchB administration markedly increased serum Ca levels and bone Ca content and decreased urinary calcium excretion in OVX-operated rats. In addition, high-dosage SchB treatment blocked osteoclastogenesis and improved trabecular bone and cartilage degeneration in the tibia of OVX-operated rats. Furthermore, high-dosage SchB treatment dramatically elevated the protein expression of phospho-PI3K, phospho-Akt and β-catenin in OVX-operated rats.

SchB exerted anti-osteoporotic activity in OVX-operated rats by accelerating the phosphorylation of PI3K and Akt, subsequently upregulating the expression of β-catenin.