Lycii radicis cortex inhibits glucocorticoid‑induced bone loss by downregulating Runx2 and BMP‑2 expression

Lycii radicis cortex (LRC) has been used to regulate high blood pressure, body temperature, pain and bone disorders in East Asia. Glucocorticoids (GCs), also known as steroids, are potent immunity regulators widely used in the treatment of inflammatory diseases. However, despite their effectiveness, GC usage is strictly controlled due to severe side‑effects, such as osteoporosis. However, further research is required as to date, at least to the best of our knowledge, there is no appropriate model to overcome secondary osteoporosis as a side‑effect of GC use. Thus, the aim of the present study was to establish an experimental model of osteoporosis induced by GC. Furthermore, the present study aimed to establish the research methodology for medical evaluations of the effectiveness and side‑effects of GCs. A secondary osteoporosis animal model was established, and the animals were divided into two groups as follows: The allergic contact dermatitis (ACD)‑induced group and the non‑ACD‑induced group. In the ACD‑induced group, a GC topical application group was compared with a GC subcutaneous injection group. The results revealed that the presence of ACD affected the induction of GC‑mediated osteoporosis. Therefore, the group exhibiting induced ACD that was treated with a topical application of GC was selected for examining the side‑effects of GCs. The effects of LRC on secondary osteoporosis were confirmed in vivo and in vitro. The results indicated that LRC regulated dexamethasone‑induced osteoblast apoptotic markers, including caspase‑6, caspase‑9, X‑linked inhibitor of apoptosis, apoptosis inhibitor 1 and apoptosis inhibitor 2, and increased the expression of osteoblast differentiation‑related genes, such as Runt‑related transcription factor 2 and bone morphogenetic protein 2 in the MC3T3E‑1 cell line. LRC also significantly reduced GC‑induced osteoporosis and exerted anti‑inflammatory effects in vivo. In addition, LRC inhibited the reduction of calbindin‑D28k in the kidney. Overall, the results of the present study suggest that the use of LRC alleviates GC‑induced secondary osteoporosis.