Xu Yuan, Ya Xiao-Ping, Zhang Wen-Jian
Department of Rheumatology, China-Japan Friendship Hospital, Beijing 100029.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Apr;32(4):521-4.
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).
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.
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).
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.
研究补肾强督方（BQR）调控强直性脊柱炎（AS）中骨保护素/核因子κB受体活化因子配体（OPG/RANKL）通路的机制。
于2009年1月至5月从中日友好医院中医风湿病科招募30例活动期AS住院或门诊患者。所有患者连续服用BQR 3个月，每日1剂，早晚各1次。此外，招募30名健康志愿者。采集患者和志愿者的血清。将成骨细胞系hFOB1.19分为3组：治疗前组、治疗后组和健康志愿者组（作为对照组）。所有细胞系用含各血清的相应培养基培养。收集成骨细胞系的上清液。采用酶联免疫吸附测定法（ELISA）检测OPG/RANKL的蛋白含量，采用逆转录聚合酶链反应（RT-PCR）检测OPG/RANKL的蛋白表达。
与对照组相比，治疗前组OPG含量、OPG的mRNA和蛋白表达、OPG/RANKL的mRNA和蛋白表达均降低，而RANKL的mRNA表达升高，差异有统计学意义（P<0.05，P<0.01）。与治疗前组相比，治疗后组OPG含量、OPG的mRNA和蛋白表达显著升高，OPG/RANKL的mRNA和蛋白表达升高，而RANKL的mRNA表达降低，差异有统计学意义（P<0.05，P<0.01）。
AS患者血清可直接抑制成骨细胞中OPG的表达，促进RANKL表达，下调OPG/RANKL比值。含BQR血清可能通过直接上调成骨细胞中OPG/RANKL比值促进成骨、抑制骨吸收，从而抑制破骨细胞的分化和功能。
