Department of Spine, Affiliated Jianhu Hospital of Xinglin College, Nantong University, Yancheng, China.
Department of Orthopedics, Shandong Public Health Clinical Center, Shandong University, Jinan, China.
J Biochem Mol Toxicol. 2024 Sep;38(9):e23797. doi: 10.1002/jbt.23797.
Osteoporosis is a common condition worldwide, affecting millions of people. Women are more commonly affected than men, and the risk increases with age. Inflammatory reaction plays a crucial role in the expansion of osteoporosis. Osteoporosis is characterized by a gradual decline in bone density and bone tissue quality, which increases fragility and raises the risk of fractures. We scrutinized the anti-osteoporosis effect of hydroxysafflor yellow A (HYA) against glucocorticoid-induced osteoporosis (GIOP) in rats. In-silico study was carried out on EGFR receptor (PDBID: 1m17), Estrogen Alpha (PDB id: 2IOG), MTOR (PDB id: 4FA6), RANKL (PDB id: 1S55), and VEGFR2 (PDB id: 1YWN) protein. For this investigation, Sprague-Dawley (SD) rats were used, and they received an oral dose of HYA (5, 10, and 20 mg/kg, b.w.) along with a subcutaneous injection of dexamethasone (0.1 mg/kg/day) to induce osteoporosis. The biomechanical, bone parameters, antioxidant, cytokines, inflammatory, nutrients, hormones, and urine parameters were estimated. HYA treatment significantly suppressed the body weight and altered the organ weight. HYA treatment remarkably suppressed the level of alkaline phosphatase, acid phosphatase, and improved the level of bone mineral density (total, proximal, mild, and dis). HYA treatment restored the level of calcium (Ca), phosphorus (P), estradiol (E), and parathyroid hormone near to the normal level. HYA treatment remarkably altered the level of biomechanical parameters, antioxidant, cytokines, urine, and inflammatory parameters. HYA treatment altered the level of osteoprotegerin (OPG), receptor activator of nuclear factor kappa beta (RANKL) and RANKL/OPG ratio. The result clearly showed the anti-osteoporosis effect of HYA against GIOP-induced osteoporosis in rats via alteration of antioxidant, cytokines, inflammatory, and bone protective parameters.
骨质疏松症是一种全球性的常见疾病，影响着数以百万计的人。女性比男性更容易受到影响，而且随着年龄的增长，风险会增加。炎症反应在骨质疏松症的扩张中起着至关重要的作用。骨质疏松症的特征是骨密度和骨组织质量逐渐下降，这增加了骨折的脆弱性和风险。我们研究了羟基红花黄色 A（HYA）对糖皮质激素诱导的骨质疏松症（GIOP）大鼠的抗骨质疏松作用。对 EGFR 受体（PDBID：1m17）、雌激素 Alpha（PDB id：2IOG）、MTOR（PDB id：4FA6）、RANKL（PDB id：1S55）和 VEGFR2（PDB id：1YWN）蛋白进行了计算机研究。为此，我们使用了 Sprague-Dawley（SD）大鼠，它们接受了 HYA（5、10 和 20mg/kg，bw）的口服剂量，以及地塞米松（0.1mg/kg/天）的皮下注射，以诱导骨质疏松症。估计了生物力学、骨参数、抗氧化剂、细胞因子、炎症、营养物质、激素和尿液参数。HYA 治疗显著抑制了体重，并改变了器官重量。HYA 治疗显著抑制了碱性磷酸酶、酸性磷酸酶的水平，并提高了骨矿物质密度（总、近端、轻度和离散）的水平。HYA 治疗使钙（Ca）、磷（P）、雌二醇（E）和甲状旁腺激素的水平恢复到正常水平。HYA 治疗显著改变了生物力学参数、抗氧化剂、细胞因子、尿液和炎症参数的水平。HYA 治疗改变了护骨素（OPG）、核因子 kappa beta 受体激活剂（RANKL）和 RANKL/OPG 比值的水平。结果清楚地表明，HYA 通过改变抗氧化剂、细胞因子、炎症和骨保护参数对 GIOP 诱导的骨质疏松症大鼠具有抗骨质疏松作用。
