Orthopaedic Center of People's Liberation Army, The Affiliated Southeast Hospital of Xiamen University, Zhangzhou, 363000, Fujian, China.
Department of Pathology, The Affiliated Southeast Hospital of Xiamen University, Zhangzhou, 363000, Fujian, China.
Biomed Pharmacother. 2018 Feb;98:280-285. doi: 10.1016/j.biopha.2017.12.072. Epub 2017 Dec 27.
Previous studies have showed that triptolide have a critical role in inhibiting osteoclast formation, bone resorption and attenuating regional osteoporosis. However, the protective role of triptolide on age-related bone loss has not been investigated. In the study, we assessed the effect of triptolide supplementation on bone microstructure and bone remolding in old male rat lumbars.
Fifty-two 22-month-old male Sprague-Dawley rats were randomly assigned to either triptolide treatment group or control group. Triptolide (15 μg/kg/d) or normal saline was administered to the rats of assigned group for 8 weeks. Lumbar bone mineral density (BMD) and bone microstructure were analyzed by micro-CT. Fluorochrome labeling of the bones was performed to measure the mineral apposition rate (MAR) and bone formation rate (BFR). Osteoclast number was also measured by TRAP staining. Plasma level of osteocalcin and tartrate-resistant acid phosphatase 5b (Tracp 5b) was also analyzed.
Micro-CT results revealed that triptolide-treated rats had significant higher BMD, bone volume over total volume (BV/TV), trabecular thickness (Tb.Th), bone trabecular number (Tb.N), and lower trabecular separation (Tb.Sp) compared to the control group. Although fluorochrome labeling result showed no significant difference in MAR and BFR between the groups, triptolide decreased osteoclast number in vivo. In addition, a significant higher level of plasma Tracp 5b was observed in the triptolide-treated rats. Furthermore, triptolide also reduced the expression of receptor for activation of NF-κB ligand (RANKL) and increased osteoprotegerin (OPG) expression in the lumbars.
These results suggested that triptolide had a protective effect on age-related bone loss at least in part by reducing osteoclast number in elder rats. Therefore, triptolide might be a feasible therapeutic approach for senile osteoporosis.
先前的研究表明雷公藤红素在抑制破骨细胞形成、骨吸收和减轻区域性骨质疏松症方面具有重要作用。然而,雷公藤红素对与年龄相关的骨丢失的保护作用尚未得到研究。在这项研究中,我们评估了雷公藤红素补充对老年雄性大鼠腰椎骨微结构和骨重塑的影响。
52 只 22 月龄雄性 Sprague-Dawley 大鼠被随机分为雷公藤红素治疗组或对照组。将雷公藤红素(15μg/kg/d)或生理盐水给予指定组的大鼠,持续 8 周。通过微 CT 分析腰椎骨密度(BMD)和骨微结构。通过荧光标记测量矿化沉积率(MAR)和骨形成率(BFR)。还通过 TRAP 染色测量破骨细胞数量。分析血浆骨钙素和抗酒石酸酸性磷酸酶 5b(Tracp 5b)水平。
微 CT 结果显示,与对照组相比,雷公藤红素治疗组大鼠的 BMD、骨体积/总体积(BV/TV)、骨小梁厚度(Tb.Th)、骨小梁数量(Tb.N)显著升高,骨小梁分离度(Tb.Sp)显著降低。虽然荧光标记结果显示两组之间 MAR 和 BFR 无显著差异,但雷公藤红素减少了体内破骨细胞数量。此外,雷公藤红素治疗组大鼠的血浆 Tracp 5b 水平显著升高。此外,雷公藤红素还降低了腰椎中核因子-κB 受体激活配体(RANKL)的表达,增加了骨保护素(OPG)的表达。
这些结果表明,雷公藤红素对老年大鼠的与年龄相关的骨丢失具有保护作用,至少部分是通过减少破骨细胞数量来实现的。因此,雷公藤红素可能是治疗老年性骨质疏松症的一种可行方法。