[The function of bushen qiangdu recipe containing serum in OPG/RANKL pathway of ankylosing spondylitis patients].

OBJECTIVE

To study the mechanism of Bushen Qiangdu Recipe (BQR) for regulating osteoprotegerin receptor activator for nuclear factor kappa B ligand (OPG/RANKL) pathway in ankylosing spondylitis (AS).

METHODS

Thirty active AS inpatients or outpatients were recruited from Department of CM Rheumatology, China-Japan Friendship Hospital from January to May 2009. All patients were treated with BQR for 3 successive months, one dose daily, once in the morning and once in the evening. Besides, 30 healthy volunteers were recruited. The serum of patients and volunteers were collected. The osteoblast cell lines hFOB1. 19 were divided into 3 groups: the pre-treatment group, the post-treatment group, and the healthy volunteer group (as the control group). All cell lines were cultured by corresponding culture medium containing each serum. The supernatant from osteoblast cell lines was collected. The protein content of OPG/RANKL was detected using ELISA, and the protein expression of OPG/RANKL was detected using RT-PCR.

RESULTS

Compared with the control group, the OPG content, the mRNA and protein expressions of OPG, and the mRNA and protein expressions of OPG/RANKL all decreased, while the mRNA expression of RANKL increased in the pre-treatment group, showing statistical difference (P<0.05, P<0.01). Compared with the pre-treatment group, the OPG content, the mRNA and protein expressions of OPG significantly increased, and the mRNA and protein expressions of OPG/RANKL increased, while the mRNA expression of RANKL decreased in the post-treatment group, showing statistical difference (P<0.05, P<0.01).

CONCLUSIONS

AS patients' serum could directly inhibit the expression of OPG in osteoblasts, promote the expression of RANKL, and down-regulate the OPG/RANKL ratio. BQR containing serum might promote the osteogenesis and inhibit the bone resorption possibly through directly up-regulating the OPG/RANKL ratio in osteoblast, thus inhibiting the differentiation and function of osteoclast.