Effects of tanshinol on markers of bone turnover in ovariectomized rats and osteoblast cultures.

Abstract

This study was aimed to explore the role of tanshinol in osteoblastic cells, and the role in vivo using an ovariectomized (OVX) rat model of osteoporosis. MC3T3-E1 cells were pretreated with 0–400 μg/mL tanshinol, and then cell viability, apoptosis, alkaline phosphatase (ALP) activity and the expressions of Collagen Type I Alpha 1 (Col1A1), Runt Related Transcription Factor 2 (Runx2) and osteocalcin (OCN) were respectively detected. Rats underwent OVX surgery was intervened with 5 mg/kg tanshinol or 25 μg/kg β-estradiol (E2) for 12 weeks. The triglycerides (TG), total cholesterol (TC), high and low density lipoprotein cholesterol (HDL-C and LDL-C), ALP, OCN and Tartrate-resistant acid phosphatase-5b (TRACP-5b) contents were measured. Besides, the expressions of main factors in nuclear factor-kappa B (NF-κB) pathway were detected. The results showed that tanshinol significantly promoted MC3T3-E1 cells viability and ALP activity, while inhibited apoptosis (P < 0.05); Col1A1, Runx2 and OCN were all up-regulated by tanshinol (P < 0.05). In OVX rats, the contents of TG, TC, LDL-C, ALP, OCN and TRACP-5b were all increased (P < 0.05), while HDL-C was decreased (P < 0.05). Tanshinol significantly alleviated these aberrant regulations (P < 0.05). Inhibitory subunit of NF-κB (IκBα) and p65 were both remarkably phosphorylated by OVX, while this phosphorylation was partially neutralized by tanshinol (P < 0.05). In conclusion, we demonstrated that tanshinol exerted a bone-protective function by modulating the markers of bone turnover possibly via blocking NF-κB pathway. This study will provide new evidence that tanshinol is a potential therapeutic option for the relief of estrogen deficiency-induced osteoporosis.